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Nemeth, Z.; Patonai, A.; Simon-Szabó, L.; Takács, I. Vitamin D and SIRT1 in Non-Communicable Diseases. Encyclopedia. Available online: https://encyclopedia.pub/entry/43461 (accessed on 19 May 2024).
Nemeth Z, Patonai A, Simon-Szabó L, Takács I. Vitamin D and SIRT1 in Non-Communicable Diseases. Encyclopedia. Available at: https://encyclopedia.pub/entry/43461. Accessed May 19, 2024.
Nemeth, Zsuzsanna, Attila Patonai, Laura Simon-Szabó, István Takács. "Vitamin D and SIRT1 in Non-Communicable Diseases" Encyclopedia, https://encyclopedia.pub/entry/43461 (accessed May 19, 2024).
Nemeth, Z., Patonai, A., Simon-Szabó, L., & Takács, I. (2023, April 25). Vitamin D and SIRT1 in Non-Communicable Diseases. In Encyclopedia. https://encyclopedia.pub/entry/43461
Nemeth, Zsuzsanna, et al. "Vitamin D and SIRT1 in Non-Communicable Diseases." Encyclopedia. Web. 25 April, 2023.
Vitamin D and SIRT1 in Non-Communicable Diseases
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This entry is adapted from the peer-reviewed paper 10.3390/ijms24076154

Vitamin D and SIRT1 have direct and indirect influence of the regulation of transcription and epigenetic changes and are related to cytoplasmic signaling pathways such as PLC/DAG/IP3/PKC/MAPK, MEK/Erk, insulin/mTOR/cell growth, proliferation; leptin/PI3K-Akt-mTORC1, Akt/NFĸB/COX-2, NFĸB/TNFα, IL-6, IL-8, IL-1β, and AMPK/PGC-1α/GLUT4, among others. Several vitamin D metabolites are generated in the liver, the kidney, and in other tissue types, which are then excreted in the urine. The most investigated and important forms are 24-hydroxylated (i.e., 24,25-dihydroxyvitamin D3, 1,24,25-trihydroxyvitamin D3); these forms are converted from 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3, respectively. CYP24A1 24-hydroxylase enzyme, which is responsible for these conversions—similarly to CYP27B1, a multicomponent enzyme in the mitochondria—is regulated by calcium, phosphorus, and 1,25-dihydroxyvitamin D3 through VDR, the receptor of vitamin D. Long-term imbalance in this system or an inappropriate amount of cytochrome P450 enzymes—which control the production, regulation, and degradation of vitamin D—can cause vitamin D insufficiency-related diseases. Thus, abnormally elevated levels of CYP24A1 can create a deficit in vitamin D levels, since this enzyme is uniquely responsible for the catabolism of vitamin D. Elevated levels of CYP24A1 are observed in breast, prostate, esophageal, colon, and lung cancers, genetically linked hypophosphatemia, diabetic nephropathy, and chronic kidney disease (CKD). Deficiency of vitamin D can also develop due to an inadequate amount of sun exposure and insufficient nutritional supplementation, or it can appear as a result of certain diseases, e.g., diabetes, cancer, chronic kidney disease, or genetically linked hypophosphatemia.

vitamin D SIRT1 metabolism epigenetics

1. Effect of Vitamin D and SIRT1 on Metabolic Syndrome

Metabolic syndrome (MetS) is defined with well-determined metabolic alterations [1][2], which serve as a favorable breeding ground and characteristic indicators for many diseases, e.g., obesity, type 2 diabetes (T2DM), CVD, hypertension, cancers, and mental disorders [3][4][5][6][7][8]. It has been shown that vitamin D deficiency is associated with T2DM development [9][10], and its level is negatively correlated with the disease state and positively with insulin sensitivity [11]. The researchers detailed above that vitamin D and SIRT1 have a significant role in a healthy lipid metabolism, as well as in the healthy relationship between metabolic/energy homeostasis and the immune system, where both are linked to regulatory molecules. Indeed, decreased vitamin D is associated with MetS as a whole, and with some components, such as obesity, increased BMI, dyslipidemia, increased blood pressure, and altered insulin and glucose metabolism [12][13]. Thus, vitamin D and SIRT1 may play a beneficial role in the prevention and complementary treatment of metabolic syndrome, since both are key molecules in metabolic/energy sensing and in immune regulation [1][2].

2. Effect of Vitamin D and SIRT1 on CVD

Vitamin D has important roles in cardiovascular health, as was mentioned above, and, in addition to other risk factors, such as smoking, high cholesterol, hypertension, obesity, and diabetes, vitamin D deficiency is connected to the occurrence of cardiovascular diseases (CVD) [14][15][16]. Although observational studies, preclinical studies, and randomized control trials all showed the beneficial effect of vitamin D on vascular and cardiac functions, linear Mendelian randomization and large clinical trials failed to demonstrate significant benefits on CKD and high-risk CVD populations [17]. However, the vast majority of these trials of vitamin D supplementation did not restrict the study populations to individuals with vitamin D deficiency and did not follow-up the changes of vitamin D level during the trial, correlating the end points with these changes [18]. Additionally, nonlinear Mendelian randomization found significant benefits of vitamin D supplementation on CVD risks [19]. However, the significant positive effect of vitamin D is widely accepted only on the reduction of CVD-related mortality [20][21][22] and all-cause mortality [23][24][25]. The micro-RNA mir34a promotes calcification in vascular smooth muscle cells by downregulation of SIRT1 and Axl [26]. An appropriate level of SIRT1 decelerates vascular calcification by affecting several osteogenic processes, including the reversal of osteogenic phenotypic transdifferentiation in vascular smooth muscle cells, upregulation of eNOS and FoxOs, activation of antioxidant properties, and enhancement of adiponectin release from perivascular adipose tissue [27]. Resveratrol and SIRT1 activators improve cardiovascular health by improving systolic blood pressure and mean arterial pressure, decreasing triglyceride, leptin, inflammation level (Il-6, IL-8, TNFα and CRP) [28], and by maintaining endothelial function and by ameliorating events related to endothelial dysfunction, e.g., impaired vasorelaxation, eNOS uncoupling, leukocyte adhesion, endothelial senescence, and endothelial mesenchymal transition [29].

3. Effect of Vitamin D and SIRT1 on CKD

Kidney function is indispensable for the synthesis of calcitriol, which allows intestinal calcium absorption in order to maintain extracellular calcium as well as phosphate levels. Therefore, the loss of kidney function leads to elevation of parathyroid hormone (PTH) and, eventually, induces hyperplastic parathyroid growth to re-establish calcium and phosphate balance [30]. The expression, activity, and regulation of 1α-hydroxylase, which is induced by PTH, hypocalcemia, and hypophosphatemia and repressed by FGF23, hyperphosphatemia, hypercalcemia, and calcitriol, is impaired in CKD [31]. The complex of calcidiol and vitamin D-binding protein (25(OH)D3/DBP) is filtered through the glomerulus from the circulation and is actively endocytosed into the proximal tubular cells by megalin, a member of the LDL receptor superfamily in the apical membrane [32]. Although PTH is upregulated in CKD, it is insufficient to restore calcitriol synthesis, as the elevated calcium and phosphate levels induce FGF23, metabolic acidosis, and PTH fragments directly inhibiting even non-renal 1α-hydroxylase expression and activity [33]. Additionally, normal kidney function is essential in the maintenance of the serum level of 25(OH)D3 for local activation by non-renal 1α-hydroxylase and the autocrine/paracrine actions of the VDR [30]. Since, in CKD, both the glomerular filtration rate (GFR) and megalin content are lower, the amount of ultrafiltrated 25(OH)D3/DBP is also lower. However, a sufficient amount of ultrafiltrated 25(OH)D3/DBP is required both for its recycling into the circulation to act as a substrate of non-renal conversion and for conversion to calcitriol in the kidney. Therefore, a vicious cycle develops [34][35][36]. Consequently, the correction of the 25(OH)D3 deficiency is necessary and sufficient in hemodialysed, and more so in anephric patients, to prevent calcitriol deficiency at an early stage of kidney disease. Moreover, epidemiological studies suggest that vitamin D deficiency is associated more strongly than calcitriol deficiency with a higher risk of disease progression and death in CKD [30]. Of note, the age-dependent decline of renal function observed over the age of 60 resulted in impaired postprandial calcium excretion. Therefore, the daily intake of vitamin D should be considered in light of this physiological decline, in order to prevent vitamin D toxicity in relation to abnormal serum and vascular calcium and phosphate homeostasis [37].
As the liver and the kidney play crucial roles in the maintenance of the active vitamin D level, liver and kidney transplant recipients more frequently develop vitamin D deficiency [38][39]. Additionally, these patients have a higher ratio of vitamin D deficiency-associated comorbidities, such as fractures, diabetes, and infections [40][41]. Since vitamin D regulates the immune system, alteration in its level affects the outcome of allografts, e.g., acute cellular rejection (ACR) and infection [42]. Similarly, several other studies reported that transplanted patients have a higher risk of infections [43][44][45][46][47] and rejections [48][49]. Thus, vitamin D supplementation and tight follow-up of its level is important in transplant recipient patients [42].

4. Effect of Vitamin D and SIRT1 on Immune System-Related Diseases

1,25(OH)2D3/VDR signaling is implicated in human innate and adaptive immune response [50][51], but it appears to be species-specific and cell-specific [52]. Based on mouse models, the beneficial effects of vitamin D are suggested in allergies, autoimmune and inflammatory diseases such as inflammatory bowel disease (IBD) [53][54][55], multiple sclerosis (MS) [56][57], autoimmune encephalomyelitis [58], diabetes [59][60][61], systemic lupus erythematosus (SLE) [62], rheumatoid arthritis (RA) [50], and asthma [63]. Prospective observational studies have found that higher vitamin D level is associated with lower rates of T2DM [64], and animal studies suggest that vitamin D promotes β-cell biosynthetic capacity and conversion of proinsulin to insulin [65]. Additionally, vitamin D increases insulin sensitivity, possibly through increased Ca2+ influx, stimulated insulin receptor expression, activation of GLUT-4 glucose transporter, and activation of peroxisome proliferator-activated receptor delta (PPAR-δ) [64][66]. However, RCTs failed to prove the positive effect of vitamin D supplementation in risk reduction of T2DM, although patients were not stratified by vitamin D deficiency and the levels of vitamin D were not continuously monitored during the follow-up, similarly to other RCTs in relation to other diseases [67][68]. A meta-analysis of observational studies found significantly decreased vitamin D levels in SLE patients compared to healthy subjects; therefore, vitamin D supplementation with regular monitoring is suggested as part of the health management of SLE patients [62]. Vitamin D induces BCAA catabolism in macrophages and leads to mTOR inhibition; however, parallel to this, it induces the expression of amino acid transporter SLC7A5 in macrophages but not in epithelial cells [52]. SLC7A5 expression level in macrophages positively correlated with clinical parameters and inflammatory conditions in RA patients, and its pharmacological blockade significantly reduced IL-1β level, a downstream target of leucin-mediated mTORC1, the signaling contributor of proinflammatory cytokine production [69]. These findings seem contradictory; however, it is possible that appropriate vitamin D levels simultaneously increase the uptake of amino acids and inhibit mTOR while SLC7A5 then fuels normal anabolic pathways. In contrast, vitamin D in a low level is likely not able to properly coordinate this metabolic network. Additionally, as synovial T cells are relatively insensitive to 1,25(OH2)D3 compared to circulating blood immune cells, treatment with vitamin D is more potent for enhancing a localized reaction in combination with other RA therapies [70][71]. Moreover, these seemingly contradictory results may have originated in the heterogeneity of this disease; of note, few studies have addressed the analysis of RA subgroups and stages [50]. Although the specific benefits of vitamin D supplementation for treatment and prevention of RA are less accepted because of inconsistent results in randomized clinical trials, conceivable benefits for the improvement of disease of RA, SLE, and osteoarthritis have been reported in meta-analyses [72]. Thus, it is advisable for patients with RA to maintain a serum 25(OH)D3 level of at least 30 ng/mL (75 nmol/mL) to prevent osteomalacia, secondary osteoporosis, and fractures [72]. In asthmatic patients, a significant reduction of exacerbation was associated with vitamin D supplementation; this was more pronounced in a subgroup of patients, where vitamin D insufficiency (<30 ng/mL) was diagnosed [63].

5. Effect of Vitamin D and SIRT1 on Cancer Cells

In relation to cancer cells, vitamin D promoted epithelial differentiation [73] and, consequently, decreased cell proliferation and differentiation in many cancer types, both by direct and indirect pathways [74][75][76]. Vitamin D induced apoptosis [77] and markedly modulated methylation, which leaded to gene repression by histone modification of the DNA [78]. Vitamin D upregulated p21WAF/CIP and p27KIP inhibitors of cell cycle arrest in colorectal cancer cells, and since the promoter region of p21 contains vitamin D response elements, calcitriol can directly regulate p21 transcription [79]. The promotion of VDR/β-catenin binding reduced the amount of β-catenin binding to T cell factor (TCF), which induces expression of E-cadherin as well as extracellular Wnt inhibitor DKK-1 [80][81][82]. CYP24A1 mitochondrial protein expression, which determines the half-life of 1,25(OH2)D3, is regulated both by its methylation status and by vitamin D. Its inhibition facilitates the antiproliferative effect of vitamin D on the downregulation of the WNT/β-catenin pathway and on the inhibition of targeted genes, e.g., c-Myc, TCF1, and LEF1 [83]. Vitamin D suppressed antiapoptotic protein expression while inducing proapoptotic protein expression on colorectal cancer cells, but not in normal colon epithelia, where it inhibited proapoptotic signaling by the downregulation of PUMA [82]. Vitamin D diminished the expression of HIF-1, VEGF, as well as IL-8, which are all important angiogenic factors [84]. Vitamin D-induced Nrf2, at a low level, can protect cells from carcinogenic ROS and inflammation, but its constitutive activation caused by mutations or pro-oncogenic signaling can protect cancer cells from cytotoxic effects of chemotherapy, creating chemoresistance [82][85]. Since there are several vitamin D target genes regulating proliferation, migration, invasiveness, differentiation, angiogenesis, extracellular matrix, or immunomodulation of cancer cell, this highlights the possible impact of an appropriate level of vitamin D on its anticancer role [74]. In a meta-analysis of cohort studies, a highly significant linear dose–response relationship was found between the overall survival of breast cancer patient and circulating 25(OH)D3 level [24]. Similarly, other prospective and retrospective epidemiological studies reported an association between a 25(OH)D3 level below 20 ng/mL and a 30–50% increased risk of colon, prostate, and breast cancer and higher mortality [86]. A systematic review found that vitamin D supplementation induced a shift in colon microbiome composition and increased its diversity [73]. In renal cancer, VDR expression is a prognostic marker and its higher expression predicted a better survival rate [87]. Resveratrol, a natural antioxidant polyphenol and dietary component which upregulates SIRT1, induced apoptosis through activation of p53 by the PI3K pathway, parallel with the inhibition of S6 ribosomal protein in breast cancer cells [88]. This dietary component inhibits estrogen-induced breast carcinogenesis as well through induction of the Nrf2-mediated pathway [89][90]. Moreover, it reverses doxorubicin-chemoresistance by the upregulation of the SIRT1/β-catenin signaling pathway [91]. Studies investigating SIRT1/vitamin D/FOXO interaction suggest a link between VDR, SIRT1, and FOXO3 function, and provide a molecular basis for the cancer chemoprevention actions of 1,25(OH2)D3 [92][93][94]. Resveratrol suppressed ovarian cancer growth and liver metastasis by inhibiting glycolysis and targeting the AMPK/mTOR pathway [95]. In addition to the beneficial effects of resveratrol on cancer cells, by inducing apoptosis under hypoxia while not affecting normal cells, it also attenuated their migratory properties through downregulation of hypoxia-induced LPA and subsequent activation of HIF-1α and VEGF signaling [96]. Resveratrol, in a cell and organ specific manner, can induce or inhibit hypoxia and ROS production, but both ultimately resulted in cell death in the cancer cells [96]. Additionally, resveratrol suppressed the production of extracellular matrix degrading and remodelling of MMP-2 and MMP-9 [97]. Resveratrol reduces the level of TNF-α, IL-1β, and IL-6 proinflammatory cytokines and suppresses STAT3 and NFκB signaling [98][99]. Moreover, it modulates non-cancer cells in the tumor microenvironment (e.g., CAFs, macrophages, T cells, and endothelial cells), facilitating their tumor-suppressive effects [96]. Resveratrol was suggested as potential alternative to NSAID and selective COX inhibitor in CRC chemoprevention, demonstrating no obvious side effects even after daily oral administration of 5 g/day for 14 days, as reported in a clinical trial [100]. Finally, a dosage ranging from 0–200 µM in combination with FOLFOX (10 µM) was sufficient to enhance antitelomeric and apoptotic potential through resensitization to chemotherapy [85][101].

References

  1. Nemeth, Z.; Kiss, E.; Takacs, I. The Role of Epigenetic Regulator SIRT1 in Balancing the Homeostasis and Preventing the Formation of Specific “Soil” of Metabolic Disorders and Related Cancers. Front. Biosci. 2022, 27, 253.
  2. Nemeth, Z.; Kiss, E.; Takacs, I. A Healthy Balance of Homeostasis by Epigenetic Regulator SIRT1 May Prevent the Development of a Specific “Soil” that Supports Metabolic Disorders and Related Cancers. In Current Overview on Disease and Health Research; Karaman, D.R., Ed.; B P International: London, UK, 2022; Volume 4, pp. 71–111.
  3. Bovolini, A.; Garcia, J.; Andrade, M.A.; Duarte, J.A. Metabolic Syndrome Pathophysiology and Predisposing Factors. Int. J. Sports Med. 2021, 42, 199–214.
  4. Litwin, M.; Kulaga, Z. Obesity, metabolic syndrome, and primary hypertension. Pediatr. Nephrol. 2021, 36, 825–837.
  5. Karra, P.; Winn, M.; Pauleck, S.; Bulsiewicz-Jacobsen, A.; Peterson, L.; Coletta, A.; Doherty, J.; Ulrich, C.M.; Summers, S.A.; Gunter, M.; et al. Metabolic dysfunction and obesity-related cancer: Beyond obesity and metabolic syndrome. Obesity 2022, 30, 1323–1334.
  6. Chasens, E.R.; Imes, C.C.; Kariuki, J.K.; Luyster, F.S.; Morris, J.L.; DiNardo, M.M.; Godzik, M.; Jeon, B.; Yang, K. Sleep and Metabolic Syndrome. Nurs. Clin. N. Am. 2021, 56, 203–217.
  7. Więckowska-Gacek, A.; Mietelska-Porowska, A.; Wydrych, M.; Wojda, U. Western diet as a trigger of Alzheimer’s disease: From metabolic syndrome and systemic inflammation to neuroinflammation and neurodegeneration. Ageing Res. Rev. 2021, 70, 101397.
  8. Kouvari, M.; D’Cunha, N.M.; Travica, N.; Sergi, D.; Zec, M.; Marx, W.; Naumovski, N. Metabolic Syndrome, Cognitive Impairment and the Role of Diet: A Narrative Review. Nutrients 2022, 14, 333.
  9. Harinarayan, C.V. Vitamin D and diabetes mellitus. Hormones 2014, 13, 163–181.
  10. Lim, S.; Kim, M.J.; Choi, S.H.; Shin, C.S.; Park, K.S.; Jang, H.C.; Billings, L.K.; Meigs, J.B. Association of vitamin D deficiency with incidence of type 2 diabetes in high-risk Asian subjects. Am. J. Clin. Nutr. 2013, 97, 524–530.
  11. Al-Timimi, D.J.; Ali, A.F. Serum 25(OH) D in Diabetes Mellitus Type 2: Relation to Glycaemic Control. J. Clin. Diagn. Res. 2013, 7, 2686–2688.
  12. Melguizo-Rodríguez, L.; Costela-Ruiz, V.; García-Recio, E.; De Luna-Bertos, E.; Ruiz, C.; Illescas-Montes, R. Role of Vitamin D in the Metabolic Syndrome. Nutrients 2021, 13, 830.
  13. Theik, N.W.Y.; Raji, O.E.; Shenwai, P.; Shah, R.; Kalluri, S.R.; Bhutta, T.H.; Hannoodee, H.; Al Khalili, M.; Khan, S. Relationship and Effects of Vitamin D on Metabolic Syndrome: A Systematic Review. Cureus 2021, 13, e17419.
  14. Latic, N.; Erben, R.G. Vitamin D and Cardiovascular Disease, with Emphasis on Hypertension, Atherosclerosis, and Heart Failure. Int. J. Mol. Sci. 2020, 21, 6483.
  15. Cosentino, N.; Campodonico, J.; Milazzo, V.; De Metrio, M.; Brambilla, M.; Camera, M.; Marenzi, G. Vitamin D and Cardiovascular Disease: Current Evidence and Future Perspectives. Nutrients 2021, 13, 3603.
  16. Lavie, C.J.; DiNicolantonio, J.J.; Milani, R.V.; O’Keefe, J.H. Vitamin D and Cardiovascular Health. Circulation 2013, 128, 2404–2406.
  17. Zittermann, A.; Trummer, C.; Theiler-Schwetz, V.; Lerchbaum, E.; März, W.; Pilz, S. Vitamin D and Cardiovascular Disease: An Updated Narrative Review. Int. J. Mol. Sci. 2021, 22, 2896.
  18. Pilz, S.; Trummer, C.; Theiler-Schwetz, V.; Grübler, M.R.; Verheyen, N.D.; Odler, B.; Karras, S.N.; Zittermann, A.; März, W. Critical Appraisal of Large Vitamin D Randomized Controlled Trials. Nutrients 2022, 14, 303.
  19. Zhou, A.; Selvanayagam, J.B.; Hyppönen, E. Non-linear Mendelian randomization analyses support a role for vitamin D deficiency in cardiovascular disease risk. Eur. Hearth J. 2022, 43, 1731–1739.
  20. Degerud, E.; Nygård, O.; De Vogel, S.; Hoff, R.; Svingen, G.F.T.; Pedersen, E.R.; Nilsen, D.W.T.; Nordrehaug, J.E.; Midttun, M.; Ueland, P.M.; et al. Plasma 25-Hydroxyvitamin D and Mortality in Patients with Suspected Stable Angina Pectoris. J. Clin. Endocrinol. Metab. 2018, 103, 1161–1170.
  21. Gaksch, M.; Jorde, R.; Grimnes, G.; Joakimsen, R.; Schirmer, H.; Wilsgaard, T.; Mathiesen, E.B.; Njølstad, I.; Løchen, M.-L.; März, W.; et al. Vitamin D and mortality: Individual participant data meta-analysis of standardized 25-hydroxyvitamin D in 26916 individuals from a European consortium. PLoS ONE 2017, 12, e0170791.
  22. Zhu, K.; Knuiman, M.; Divitini, M.; Hung, J.; Lim, E.M.; Cooke, B.R.; Walsh, J.P. Serum 25-hydroxyvitamin D as a predictor of mortality and cardiovascular events: A 20-year study of a community-based cohort. Clin. Endocrinol. 2018, 88, 154–163.
  23. Al-Khalidi, B.; Kimball, S.M.; Kuk, J.L.; Ardern, C.I. Metabolically healthy obesity, vitamin D, and all-cause and cardiometabolic mortality risk in NHANES III. Clin. Nutr. 2019, 38, 820–828.
  24. Hu, K.; Callen, D.F.; Li, J.; Zheng, H. Circulating Vitamin D and Overall Survival in Breast Cancer Patients: A Dose-Response Meta-Analysis of Cohort Studies. Integr. Cancer Ther. 2018, 17, 217–225.
  25. Sun, Y.-Q.; Langhammer, A.; Skorpen, F.; Chen, Y.; Mai, X.-M. Serum 25-hydroxyvitamin D level, chronic diseases and all-cause mortality in a population-based prospective cohort: The HUNT Study, Norway. BMJ Open 2017, 7, e017256.
  26. Badi, I.; Mancinelli, L.; Polizzotto, A.; Ferri, D.; Zeni, F.; Burba, I.; Milano, G.; Brambilla, F.; Saccu, C.; Bianchi, M.E.; et al. miR-34a Promotes Vascular Smooth Muscle Cell Calcification by Downregulating SIRT1 (Sirtuin 1) and Axl (AXL Receptor Tyrosine Kinase). Arter. Thromb. Vasc. Biol. 2018, 38, 2079–2090.
  27. Lu, C.-L.; Liao, M.-T.; Hou, Y.-C.; Fang, Y.-W.; Zheng, C.-M.; Liu, W.-C.; Chao, C.-T.; Lu, K.-C.; Ng, Y.-Y. Sirtuin-1 and Its Relevance in Vascular Calcification. Int. J. Mol. Sci. 2020, 21, 1593.
  28. Timmers, S.; Konings, E.; Bilet, L.; Houtkooper, R.H.; van de Weijer, T.; Goossens, G.H.; Hoeks, J.; van der Krieken, S.; Ryu, D.; Kersten, S.; et al. Calorie Restriction-like Effects of 30 Days of Resveratrol Supplementation on Energy Metabolism and Metabolic Profile in Obese Humans. Cell Metab. 2011, 14, 612–622.
  29. Parsamanesh, N.; Asghari, A.; Sardari, S.; Tasbandi, A.; Jamialahmadi, T.; Xu, S.; Sahebkar, A. Resveratrol and endothelial function: A literature review. Pharmacol. Res. 2021, 170, 105725.
  30. Dusso, A.S.; Slatopolsky, E. Chapter 70—Vitamin D and Renal Disease. In Vitamin D, 3rd ed.; Feldman, D., Pike, J.W., Adams, J.S., Eds.; Academic Press: San Diego, CA, USA, 2011; pp. 1325–1357.
  31. Dusso, A.S.; Brown, A.J.; Slatopolsky, E. Vitamin D. Am. J. Physiol. Renal. Physiol. 2005, 289, F8–F28.
  32. Nykjaer, A.; Dragun, D.; Walther, D.; Vorum, H.; Jacobsen, C.; Herz, J.; Melsen, F.; Christensen, E.I.; E Willnow, T. An Endocytic Pathway Essential for Renal Uptake and Activation of the Steroid 25-(OH) Vitamin D3. Cell 1999, 96, 507–515.
  33. Usatii, M.; Rousseau, L.; Demers, C.; Petit, J.-L.; Brossard, J.-H.; Gascon-Barré, M.; Lavigne, J.; Zahradnik, R.; Nemeth, E.; D’Amour, P. Parathyroid hormone fragments inhibit active hormone and hypocalcemia-induced 1,25(OH)2D synthesis. Kidney Int. 2007, 72, 1330–1335.
  34. Al-Badr, W.; Martin, K.J. Vitamin D and Kidney Disease. Clin. J. Am. Soc. Nephrol. 2008, 3, 1555–1560.
  35. Al-Aly, Z.; Qazi, R.A.; González, E.A.; Zeringue, A.; Martin, K.J. Changes in Serum 25-Hydroxyvitamin D and Plasma Intact PTH Levels Following Treatment with Ergocalciferol in Patients With CKD. Am. J. Kidney Dis. 2007, 50, 59–68.
  36. Liu, W.; Yu, W.R.; Carling, T.; Juhlin, C.; Rastad, J.; Ridefelt, P.; Akerström, G.; Hellman, P. Regulation of gp330/megalin expression by vitamins A and D. Eur. J. Clin. Investig. 1998, 28, 100–107.
  37. Towler, D.A. Chapter 73—Vitamin D: Cardiovascular Effects and Vascular Calcification. In Vitamin D, 3rd ed.; Feldman, D., Pike, J.W., Adams, J.S., Eds.; Academic Press: San Diego, CA, USA, 2011; pp. 1403–1426.
  38. Yin, S.; Wang, X.; Li, L.; Huang, Z.; Fan, Y.; Song, T.; Lin, T. Prevalence of vitamin D deficiency and impact on clinical outcomes after kidney transplantation: A systematic review and meta-analysis. Nutr. Rev. 2022, 80, 950–961.
  39. Stein, E.M.; Shane, E. Chapter 68—Vitamin D and Organ Transplantation. In Vitamin D, 3rd ed.; Feldman, D., Pike, J.W., Adams, J.S., Eds.; Academic Press: San Diego, CA, USA, 2011; pp. 1291–1298.
  40. Guichelaar, M.M.J.; Schmoll, J.; Malinchoc, M.; Hay, J.E. Fractures and avascular necrosis before and after orthotopic liver transplantation: Long-term follow-up and predictive factors. Hepatology 2007, 46, 1198–1207.
  41. Oufroukhi, L.; Kamar, N.; Muscari, F.; Lavayssière, L.; Guitard, J.; Ribes, D.; Esposito, L.; Alric, L.; Hanaire, H.; Rostaing, L. Predictive Factors for Posttransplant Diabetes Mellitus Within One-Year of Liver Transplantation. Transplantation 2008, 85, 1436–1442.
  42. Zhou, Q.; Li, L.; Chen, Y.; Zhang, J.; Zhong, L.; Peng, Z.; Xing, T. Vitamin D supplementation could reduce the risk of acute cellular rejection and infection in vitamin D deficient liver allograft recipients. Int. Immunopharmacol. 2019, 75, 105811.
  43. Fernández-Ruiz, M.; Corbella, L.; Morales-Cartagena, A.; González, E.; Polanco, N.; Ruiz-Merlo, T.; Parra, P.; Silva, J.T.; López-Medrano, F.; Juan, R.S.; et al. Vitamin D deficiency and infection risk in kidney transplant recipients: A single-center cohort study. Transpl. Infect. Dis. 2018, 20, e12988.
  44. Schreiber, P.W.; Bischoff-Ferrari, H.A.; Boggian, K.; van Delden, C.; Enriquez, N.; Fehr, T.; Garzoni, C.; Hirsch, H.H.; Hirzel, C.; Manuel, O.; et al. Vitamin D status and risk of infections after liver transplantation in the Swiss Transplant Cohort Study. Transpl. Int. 2019, 32, 49–58.
  45. Fernández-Ruiz, M.; Rodríguez-Goncer, I.; Ruiz-Merlo, T.; Parra, P.; López-Medrano, F.; Andrés, A.; Aguado, J.M. Low 25-hydroxyvitamin D Levels and the Risk of Late CMV Infection After Kidney Transplantation: Role for CMV-specific Mediated Immunity. Transplantation 2019, 103, e216–e217.
  46. Kalluri, H.V.; Sacha, L.M.; Ingemi, A.; Shullo, M.A.; Johnson, H.J.; Sood, P.; Tevar, A.D.; Humar, A.; Venkataramanan, R. Low vitamin D exposure is associated with higher risk of infection in renal transplant recipients. Clin. Transplant. 2017, 31, e12955.
  47. Kwon, Y.E.; Kim, H.; Oh, H.J.; Park, J.T.; Han, S.H.; Ryu, D.-R.; Yoo, T.-H.; Kang, S.-W. Vitamin D Deficiency Is an Independent Risk Factor for Urinary Tract Infections After Renal Transplants. Medicine 2015, 94, e594.
  48. Mirzakhani, M.; Mohammadkhani, S.; Hekmatirad, S.; Aghapour, S.; Gorjizadeh, N.; Shahbazi, M.; Mohammadnia-Afrouzi, M. The association between vitamin D and acute rejection in human kidney transplantation: A systematic review and meta-analysis study. Transpl. Immunol. 2021, 67, 101410.
  49. Lowery, E.M.; Bemiss, B.; Cascino, T.; Durazo-Arvizu, R.A.; Forsythe, S.M.; Alex, C.; Laghi, F.; Love, R.B.; Camacho, P. Low vitamin D levels are associated with increased rejection and infections after lung transplantation. J. Heart Lung Transplant. 2012, 31, 700–707.
  50. Harrison, S.R.; Li, D.; Jeffery, L.E.; Raza, K.; Hewison, M. Vitamin D, Autoimmune Disease and Rheumatoid Arthritis. Calcif. Tissue Int. 2020, 106, 58–75.
  51. van Etten, E.; Mathieu, C. Immunoregulation by 1,25-dihydroxyvitamin D3: Basic concepts. J. Steroid Biochem. Mol. Biol. 2005, 97, 93–101.
  52. Dimitrov, V.; Barbier, C.; Ismailova, A.; Wang, Y.; Dmowski, K.; Salehi-Tabar, R.; Memari, B.; Groulx-Boivin, E.; White, J.H. Vitamin D-regulated Gene Expression Profiles: Species-specificity and Cell-specific Effects on Metabolism and Immunity. Endocrinology 2021, 162, bqaa218.
  53. Kong, J.; Zhang, Z.; Musch, M.W.; Ning, G.; Sun, J.; Hart, J.; Bissonnette, M.; Li, Y.C. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am. J. Physiol. Gastrointest. Liver Physiol. 2008, 294, G208–G216.
  54. Lagishetty, V.; Misharin, A.V.; Liu, N.Q.; Lisse, T.S.; Chun, R.F.; Ouyang, Y.; McLachlan, M.; Adams, S.; Hewison, M. Vitamin D deficiency in mice impairs colonic antibacterial activity and predisposes to colitis. Endocrinology 2010, 151, 2423–2432.
  55. Meeker, S.; Seamons, A.; Paik, J.; Treuting, P.M.; Brabb, T.; Grady, W.M.; Maggio-Prince, L. Increased Dietary Vitamin D Suppresses MAPK Signaling, Colitis, and Colon Cancer. Cancer Res. 2014, 74, 4398–4408.
  56. Speer, G. Impact of vitamin D in neurological diseases and neurorehabilitation: From dementia to multiple sclerosis. Part I: The role of vitamin D in the prevention and treatment of multiple sclerosis. Ideggyogy Sz. 2013, 66, 293–303.
  57. de Carvalho, J.F.; Pereira, R.M.; Shoenfeld, Y. Pearls in autoimmunity. Auto Immun. Highlights 2011, 2, 1–4.
  58. van Etten, E.; Gysemans, C.; Branisteanu, D.D.; Verstuyf, A.; Bouillon, R.; Overbergh, L.; Mathieu, C. Novel insights in the immune function of the vitamin D system: Synergism with interferon-beta. J. Steroid Biochem. Mol. Biol. 2007, 103, 546–551.
  59. Gregori, S.; Giarratana, N.; Smiroldo, S.; Uskokovic, M.; Adorini, L. A 1α,25-Dihydroxyvitamin D3 Analog Enhances Regulatory T-Cells and Arrests Autoimmune Diabetes in NOD Mice. Diabetes 2002, 51, 1367–1374.
  60. Mathieu, C.; Waer, M.; Laureys, J.; Rutgeerts, O.; Bouillon, R. Prevention of autoimmune diabetes in NOD mice by 1,25 dihydroxyvitamin D3. Diabetologia 1994, 37, 552–558.
  61. Takiishi, T.; Ding, L.; Baeke, F.; Spagnuolo, I.; Sebastiani, G.; Laureys, J.; Verstuyf, A.; Carmeliet, G.; Dotta, F.; Van Belle, T.L.; et al. Dietary Supplementation with High Doses of Regular Vitamin D3 Safely Reduces Diabetes Incidence in NOD Mice When Given Early and Long Term. Diabetes 2014, 63, 2026–2036.
  62. Islam, A.; Khandker, S.S.; Alam, S.S.; Kotyla, P.; Hassan, R. Vitamin D status in patients with systemic lupus erythematosus (SLE): A systematic review and meta-analysis. Autoimmun. Rev. 2019, 18, 102392.
  63. Wang, M.; Liu, M.; Wang, C.; Xiao, Y.; An, T.; Zou, M.; Cheng, G. Association between vitamin D status and asthma control: A meta-analysis of randomized trials. Respir. Med. 2019, 150, 85–94.
  64. Mitri, J.; Pittas, A.G. Vitamin D and diabetes. Endocrinol. Metab. Clin. N. Am. 2014, 43, 205–232.
  65. Grammatiki, M.; Rapti, E.; Karras, S.; Ajjan, R.A.; Kotsa, K. Vitamin D and diabetes mellitus: Causal or casual association? Rev. Endocr. Metab. Disord. 2017, 18, 227–241.
  66. Maestro, B.; Campion, J.; Dávila, N.; Calle, C. Stimulation by 1,25-Dihydroxyvitamin D3 of Insulin Receptor Expression and Insulin Responsiveness for Glucose Transport in U-937 Human Promonocytic Cells. Endocr. J. 2000, 47, 383–391.
  67. Pittas, A.G.; Dawson-Hughes, B.; Sheehan, P.; Ware, J.H.; Knowler, W.C.; Aroda, V.R.; Brodsky, I.; Ceglia, L.; Chadha, C.; Chatterjee, R.; et al. Vitamin D Supplementation and Prevention of Type 2 Diabetes. N. Engl. J. Med. 2019, 381, 520–530.
  68. Sacerdote, A.; Dave, P.; Lokshin, V.; Bahtiyar, G. Type 2 Diabetes Mellitus, Insulin Resistance, and Vitamin D. Curr. Diab. Rep. 2019, 19, 101.
  69. Yoon, B.R.; Oh, Y.-J.; Kang, S.W.; Lee, E.B.; Lee, W.-W. Role of SLC7A5 in Metabolic Reprogramming of Human Monocyte/Macrophage Immune Responses. Front. Immunol. 2018, 9, 53.
  70. Jeffery, L.E.; Henley, P.; Marium, N.; Filer, A.; Sansom, D.M.; Hewison, M.; Raza, K. Decreased sensitivity to 1,25-dihydroxyvitamin D3 in T cells from the rheumatoid joint. J. Autoimmun. 2018, 88, 50–60.
  71. Gardner, D.H.; Jeffery, L.E.; Soskic, B.; Briggs, Z.; Hou, T.Z.; Raza, K.; Sansom, D.M. 1,25(OH)2D3 Promotes the Efficacy of CD28 Costimulation Blockade by Abatacept. J. Immunol. 2015, 195, 2657–2665.
  72. Charoenngam, N. Vitamin D and Rheumatic Diseases: A Review of Clinical Evidence. Int. J. Mol. Sci. 2021, 22, 10659.
  73. Na, S.-Y.; Kim, K.B.; Lim, Y.J.; Song, H.J. Vitamin D and Colorectal Cancer: Current Perspectives and Future Directions. J. Cancer Prev. 2022, 27, 147–156.
  74. Carlberg, C.; Muñoz, A. An update on vitamin D signaling and cancer. Semin. Cancer Biol. 2022, 79, 217–230.
  75. Trump, D.L. Calcitriol and cancer therapy: A missed opportunity. Bone Rep. 2018, 9, 110–119.
  76. Watanabe, R.; Inoue, D. Current Topics on Vitamin D. Anti-cancer effects of vitamin D. Clin. Calcium. 2015, 25, 373–380.
  77. Giammanco, M.; Di Majo, D.; La Guardia, M.; Aiello, S.; Crescimannno, M.; Flandina, C.; Tumminello, F.M.; Leto, G. Vitamin D in cancer chemoprevention. Pharm. Biol. 2015, 53, 1399–1434.
  78. Ramnath, N.; Nadal, E.; Jeon, C.K.; Sandoval, J.; Colacino, J.; Rozek, L.S.; Christensen, P.J.; Esteller, M.; Beer, D.G.; Kim, S.H. Epigenetic Regulation of Vitamin D Metabolism in Human Lung Adenocarcinoma. J. Thorac. Oncol. 2014, 9, 473–482.
  79. Scaglione-Sewell, B.A.; Bissonnette, M.; Skarosi, S.; Abraham, C.; Brasitus, T.A. A vitamin D3 analog induces a G1-phase arrest in CaCo-2 cells by inhibiting cdk2 and cdk6: Roles of cyclin E, p21Waf1, and p27Kip1. Endocrinology 2000, 141, 3931–3939.
  80. Razak, S.; Afsar, T.; Almajwal, A.; Alam, I.; Jahan, S. Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): Involvement of Wnt/beta-catenin and other signal transduction pathways. Cell Biosci. 2019, 9, 15.
  81. Beildeck, M.E.; Islam, M.; Shah, S.; Welsh, J.; Byers, S.W. Control of TCF-4 Expression by VDR and Vitamin D in the Mouse Mammary Gland and Colorectal Cancer Cell Lines. PLoS ONE 2009, 4, e7872.
  82. Muñoz, A.; Grant, W.B. Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms. Nutrients 2022, 14, 1448.
  83. Sun, H.; Jiang, C.; Cong, L.; Wu, N.; Wang, X.; Hao, M.; Liu, T.; Wang, L.; Liu, Y.; Cong, X. CYP24A1 Inhibition Facilitates the Antiproliferative Effect of 1,25(OH)(2)D(3) Through Downregulation of the WNT/beta-Catenin Pathway and Methylation-Mediated Regulation of CYP24A1 in Colorectal Cancer Cells. DNA Cell Biol. 2018, 37, 742–749.
  84. El-Sharkawy, A.; Malki, A. Vitamin D Signaling in Inflammation and Cancer: Molecular Mechanisms and Therapeutic Implications. Molecules 2020, 25, 3219.
  85. Scuto, M.; Salinaro, A.T.; Caligiuri, I.; Ontario, M.L.; Greco, V.; Sciuto, N.; Crea, R.; Calabrese, E.J.; Rizzolio, F.; Canzonieri, V.; et al. Redox modulation of vitagenes via plant polyphenols and vitamin D: Novel insights for chemoprevention and therapeutic interventions based on organoid technology. Mech. Ageing Dev. 2021, 199, 111551.
  86. Wang, H.; Chen, W.; Li, D.; Yin, X.; Zhang, X.; Olsen, N.; Zheng, S.G. Vitamin D and Chronic Diseases. Aging Dis. 2017, 8, 346–353.
  87. The Human Protein Atlas: VDR. Available online: http://www.proteinatlas.org/ENSG00000111424-VDR/tissue (accessed on 19 August 2022).
  88. Alkhalaf, M. Resveratrol-Induced Apoptosis Is Associated with Activation of p53 and Inhibition of Protein Translation in T47D Human Breast Cancer Cells. Pharmacology 2007, 80, 134–143.
  89. Singh, B.; Shoulson, R.; Chatterjee, A.; Ronghe, A.; Bhat, N.K.; Dim, D.C.; Bhat, H.K. Resveratrol inhibits estrogen-induced breast carcinogenesis through induction of NRF2-mediated protective pathways. Carcinogenesis 2014, 35, 1872–1880.
  90. Zhou, X.; Zhao, Y.; Wang, J.; Wang, X.; Chen, C.; Yin, D.; Zhao, F.; Yin, J.; Guo, M.; Zhang, L.; et al. Resveratrol represses estrogen-induced mammary carcinogenesis through NRF2-UGT1A8-estrogen metabolic axis activation. Biochem. Pharmacol. 2018, 155, 252–263.
  91. Jin, X.; Wei, Y.; Liu, Y.; Lu, X.; Ding, F.; Wang, J.; Yang, S. Resveratrol promotes sensitization to Doxorubicin by inhibiting epithelial-mesenchymal transition and modulating SIRT1/beta-catenin signaling pathway in breast cancer. Cancer Med. 2019, 8, 1246–1257.
  92. An, B.-S.; Tavera-Mendoza, L.E.; Dimitrov, V.; Wang, X.; Calderon, M.R.; Wang, H.-J.; White, J.H. Stimulation of Sirt1-Regulated FoxO Protein Function by the Ligand-Bound Vitamin D Receptor. Mol. Cell. Biol. 2010, 30, 4890–4900.
  93. An, B.; Tavera-Mendoza, L.; Dimitrov, V.; White, J. Stimulation of Sirt1-Regulated FoxO Protein Function by the Hormone-Bound Vitamin D Receptor. In Endocrine Reviews; Endocrine Society: Chevy Chase, MD, USA, 2010; Volume 31.
  94. Chen, H.Y.; Hu, X.Q.; Yang, R.L.; Wu, G.P.; Tan, Q.; Goltzman, D.; Miao, D. SIRT1/FOXO3a axis plays an important role in the prevention of mandibular bone loss induced by 1,25(OH)(2)D deficiency. Int. J. Biol. Sci. 2020, 16, 2712–2726.
  95. Liu, Y.; Tong, L.; Luo, Y.; Li, X.; Chen, G.; Wang, Y. Resveratrol inhibits the proliferation and induces the apoptosis in ovarian cancer cells via inhibiting glycolysis and targeting AMPK/mTOR signaling pathway. J. Cell. Biochem. 2018, 119, 6162–6172.
  96. Han, Y.; Jo, H.; Cho, J.H.; Dhanasekaran, D.N.; Song, Y.S. Resveratrol as a Tumor-Suppressive Nutraceutical Modulating Tumor Microenvironment and Malignant Behaviors of Cancer. Int. J. Mol. Sci. 2019, 20, 925.
  97. Gweon, E.J.; Kim, S.-J. Resveratrol attenuates matrix metalloproteinase-9 and -2-regulated differentiation of HTB94 chondrosarcoma cells through the p38 kinase and JNK pathways. Oncol. Rep. 2014, 32, 71–78.
  98. Chen, L.; Liu, T.; Wang, Q.; Liu, J. Anti-inflammatory effect of combined tetramethylpyrazine, resveratrol and curcumin in vivo. BMC Complement. Altern. Med. 2017, 17, 233.
  99. Qi, B.; Shi, C.; Meng, J.; Xu, S.; Liu, J. Resveratrol alleviates ethanol-induced neuroinflammation in vivo and in vitro: Involvement of TLR2-MyD88-NF-κB pathway. Int. J. Biochem. Cell Biol. 2018, 103, 56–64.
  100. Patel, K.R.; Brown, V.A.; Jones, D.J.; Britton, R.G.; Hemingway, D.; Miller, A.S.; West, K.P.; Booth, T.D.; Perloff, M.; Crowell, J.A.; et al. Clinical Pharmacology of Resveratrol and Its Metabolites in Colorectal Cancer Patients. Cancer Res. 2010, 70, 7392–7399.
  101. Chung, S.S.; Dutta, P.; Austin, D.; Wang, P.; Awad, A.; Vadgama, J.V. Combination of resveratrol and 5-flurouracil enhanced anti-telomerase activity and apoptosis by inhibiting STAT3 and Akt signaling pathways in human colorectal cancer cells. Oncotarget 2018, 9, 32943–32957.
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Subjects: Endocrinology & Metabolism
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Zsuzsanna Nemeth
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Attila Patonai
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Laura Simon-Szabó
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István Takács
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Update Date: 28 Apr 2023
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