Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 1716 2022-11-06 21:07:04 |
2 layout Meta information modification 1716 2022-11-09 01:46:49 | |
3 layout Meta information modification 1716 2022-11-10 08:47:10 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Alfaqih, M.S.;  Tarawan, V.M.;  Sylviana, N.;  Goenawan, H.;  Lesmana, R.;  Susianti, S. Effects of Vitamin D on Satellite Cells. Encyclopedia. Available online: (accessed on 19 June 2024).
Alfaqih MS,  Tarawan VM,  Sylviana N,  Goenawan H,  Lesmana R,  Susianti S. Effects of Vitamin D on Satellite Cells. Encyclopedia. Available at: Accessed June 19, 2024.
Alfaqih, Muhammad Subhan, Vita Murniati Tarawan, Nova Sylviana, Hanna Goenawan, Ronny Lesmana, Susianti Susianti. "Effects of Vitamin D on Satellite Cells" Encyclopedia, (accessed June 19, 2024).
Alfaqih, M.S.,  Tarawan, V.M.,  Sylviana, N.,  Goenawan, H.,  Lesmana, R., & Susianti, S. (2022, November 08). Effects of Vitamin D on Satellite Cells. In Encyclopedia.
Alfaqih, Muhammad Subhan, et al. "Effects of Vitamin D on Satellite Cells." Encyclopedia. Web. 08 November, 2022.
Effects of Vitamin D on Satellite Cells

Vitamin D is a micronutrient that plays a role in the homeostasis of various body organs, including skeletal muscle. Skeletal muscle growth and regeneration are critically affected by satellite cells, skeletal muscle stem cells. The discovery of vitamin D receptors on satellite cells supports the role of vitamin D in regulating satellite cell function. In vivo studies have shown the effect of vitamin D on skeletal muscle growth in early life, muscle homeostasis in aging, and skeletal muscle regeneration in conditions of muscle injury or chronic disease.

vitamin D satellite cells skeletal muscle in vivo

1. Introduction

Vitamin D is a prohormone that has two main inactive isoforms, namely vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) [1]. Vitamin D2 is obtained from ultraviolet (UV) irradiation of ergosterol, a steroid that is found in some plants and fungi. Meanwhile, vitamin D3 is obtained mainly from UV irradiation of 7-dehydrocholesterol in the skin [2][3]. In addition, vitamin D3 is also obtained to a small extent from dietary intake such as oily fish, meat, or egg [1]
Vitamin D either obtained from UV exposure or food is then hydroxylated in the liver by vitamin D-25-hydroxylase to become 25-hydroxyvitamin D (25(OH)D) or also called calcidiol. 25(OH)D is a stable metabolite in the blood and best reflects exposure and absorption of Vitamin D. Therefore, 25(OH)D is used as an indicator of vitamin D status [1][4]. Furthermore, 25(OH)D needs to be converted by the enzyme 25(OH)D-1-OHase (CYP27B1) in the kidneys to become 1.25-dihydroxyvitamin D (1.25(OH)2D), the active form of vitamin D or also called calcitriol [5].
The classical function of vitamin D that has long been recognized is its role in the regulation of calcium and phosphate homeostasis and bone metabolism [6][7]. In the last few decades, some studies have indicated the non-classical function of vitamin D in various organs including skeletal muscle [8][9].
Satellite cells are skeletal muscle stem cells located between the basal lamina and sarcolemma which play a pivotal role in skeletal muscle growth and regeneration [10][11]. In homeostatic condition, satellite cells typically are in a quiescent state. The satellite cells will be activated when there are stimuli for skeletal muscle regeneration or hypertrophy, such as during an injury or exercise. Activated satellite cells will become myoblasts which proliferate and differentiate further to form new muscle fibers or fuse with preexisting muscle fibers [11][12]. This process is regulated by several myogenic regulatory factors (such as Myf5, MyoD, MRF4, and myogenin) [13][14]. In addition, some activated satellite cells can also undergo self-renewal and return to a quiescent state to replenish the satellite cell population (Figure 1) [15].
Figure 1. Satellite cells’ activity in skeletal muscle regeneration. Under homeostatic conditions, satellite cells are typically in a quiescent state and express Pax7. Notch signaling plays a role in maintaining the quiescent state of satellite cells. When there are stimuli for skeletal muscle regeneration, various myogenic regulatory factors (Myf5, MyoD, myogenin, and MRF4) regulate satellite cells’ activation, proliferation, and differentiation to form new muscle fibers. Some satellite cells will undergo self-renewal and return to a quiescent state to replenish the satellite cell population. Notch signaling through its regulation of Pax7 plays a role in promoting satellite cell self-renewal.
Several studies have shown that satellite cells express vitamin D receptor (VDR) [16][17][18]. Therefore, vitamin D may play a role in regulating satellite cells’ activity and function. A previous systematic review has discussed the effects of active vitamin D on myogenesis in vitro [19]. However, in vitro models cannot fully mimic the microenvironment of in vivo models [20][21]. Satellite cells’ fate is strongly influenced by their niche. Signals and properties of muscle fibers, basal lamina, as well as microvasculature, and surrounding interstitial cells influence the regulation of satellite cells’ function [22]. When satellite cells are removed from their in vivo niche and cultured in vitro, the satellite cells are activated and committed to proliferation and differentiation, thereby losing their stem cell properties [23]. This research discusses the latest evidence from in vivo studies regarding the role of vitamin D on satellite cells.

2. Effects of Vitamin D on Satellite Cells

In the neonatal period, skeletal muscle undergoes a high growth rate that involves high protein synthesis accompanied by a rapid increase in myonuclei. Satellite cells contribute to the addition of myonuclei to growing muscle fibers in the postnatal period [24]. This process of skeletal muscle growth depends on the proliferation of satellite cells. In 4-day-old rats with a chronically unloaded hindlimb, there was impaired growth of the soleus muscle associated with a decrease in mitotically active satellite cells [25]. The rapid growth of skeletal muscle during early life requires adequate nutrition. Nutrition has a critical influence in providing components for muscle mass synthesis and various signaling involved in the muscle fiber anabolism [24].
Vitamin D is a micronutrient that plays a role in maintaining various body functions throughout life [26]. Srikuea et al. demonstrated that satellite cells are the target cells of vitamin D action and the response of satellite cells to vitamin D varies depending on age. There is a decrease in satellite cell response to vitamin D in aged muscles compared to muscles in the developmental age [18]. These findings support the importance of vitamin D signaling in early life when satellite cell activity is high. Improved vitamin D status is associated with increased proliferation and myogenic capacity of satellite cells in the early weeks of life[27][28]. However, studies do not support the effect of vitamin D signaling on satellite cell number during muscle growth in the early life period [27][29]. A possible explanation is that the high rate of satellite cell proliferation in the early life period plays a role in providing new myonuclei to growing muscles and not increasing the number of satellite cell reserves.
Acute injury involves sudden changes in the form of damage to muscle fibers, infiltration of inflammatory cells, edema, and damage to surrounding tissues. All of these lead to a change in the niche and trigger the activation of satellite cells [30]. Vitamin D signaling appears to influence satellite cells’ function in skeletal muscle regeneration. In mice with vitamin D deficiency, there was a decrease in markers of activation and differentiation of satellite cells [31]. However, high-dose vitamin D supplementation without considering baseline vitamin D status leads to impaired satellite cell differentiation, delayed muscle fiber formation, and fibrosis formation in regenerating muscle [32]. Dosing appears to be a crucial issue when administering vitamin D during muscle regeneration. In vitro studies suggest that the administration of vitamin D supports muscle regeneration in a dose-dependent manner. However, at very high doses, it inhibits muscle formation [33][34][35]. The exact mechanism of the effect of various doses of vitamin D on the satellite cells' function in skeletal muscle regeneration needs to be explored further.
In aging, there are some changes in the satellite cell niche, which causes the satellite cells to lose their quiescence and tend to differentiate prematurely [36]. Exposure of satellite cells in aging mice with serum from young mice can restore the regenerative function of satellite cells [[37]. Aging is associated with decreased Notch signaling, a master regulator in maintaining the quiescent state of satellite cells[36]. Decreased Notch signaling in aged rats with vitamin D deficiency suggests that vitamin D may play a role in the regulation of Notch signaling in aging [38]. In in vitro study, Olsson et al. showed that the administration of vitamin D to human-derived myoblasts increased Hes1 mRNA expression, the gene target of Notch signaling [39]. One possible mechanism for vitamin D to regulate Notch signaling is its role in increasing Forkhead box O3 (FOXO3) expression [39]. A previous study demonstrated that FOXO3 is expressed in quiescent satellite cells. FOXO3 modulates Notch signaling by directly increasing Notch receptor expression. The FOXO3-Notch axis is required for satellite cell self-renewal by restoring satellite cell quiescence in regenerating muscle[40].
Vitamin D deficiency in aged rats was also associated with decreased Bmp4 and Fgf2 mRNA expression [38]. BMP signaling plays a role in increasing the satellite cell pool by promoting satellite cell proliferation and preventing precocious differentiation [41]. Stantzou et al. showed that inhibition of BMP signaling decreases the satellite cell pool [42]. Meanwhile, Fgf2 enhances satellite cell proliferation without suppressing differentiation [43]. Faria et al. assumed that the aged rats in their study experienced discrete regeneration episodes due to daily damage, so satellite cell proliferation was needed [38]. In another study, Fgf2 expression increased in aging muscle and triggered satellite cell proliferation and myogenic differentiation in homeostatic conditions. This causes satellite cell depletion and reduced muscle regeneration capacity [44]. Further studies are needed to confirm the role of vitamin D supplementation on Fgf2 in aged rats.
In chronic illness, there may be a chronic injury to the muscle depending on the severity and type of disease. Alterations in energy metabolism, inflammation, or restriction of movement can be factors that cause changes in satellite cells’ activity in diseased states [45][46]. Han et al. reported that an increase in extracellular adenosine (eADO) in diabetic mice decreased the regenerative function of satellite cells [47]. Satellite cells cultured on a high-glucose medium showed decreased proliferation and expression of Pax7, MyoD, and myogenin proteins [48]. In diseased experimental animal models, vitamin D deficiency aggravates the impaired function of satellite cells. Meanwhile, vitamin D supplementation ameliorates the impaired function of these satellite cells. Thus, it is important to pay attention to vitamin D status in various chronic diseases. 

3. Conclusion and Future Perspectives

In vivo studies support a direct role of vitamin D on satellite cells’ function during muscle growth, injury, aging, or chronic disease. Vitamin D appears to increase satellite cell proliferation in the early life period during rapid muscle growth. Adequate vitamin D status is required to support the satellite cells’ function in skeletal muscle regeneration during acute injury. However, the administration of high doses of vitamin D decreases satellite cell differentiation and delays new muscle fiber formation. Vitamin D deficiency in aging was associated with the decrease in Notch signaling resulting in satellite cells losing their quiescent and differentiating prematurely. Vitamin D supplementation ameliorates the impairment of satellite cell function in chronic disease. Thus, to provide optimal effects on satellite cells’ function, it is necessary to administer vitamin D at a dose according to the physiological needs of each individual. Further research is needed to determine the most appropriate dose and duration of vitamin D supplementation in the various age groups and specific conditions such as in early life, injury, aging, or chronic disease.


  1. Ran Zhang; Declan P Naughton; Vitamin D in health and disease: Current perspectives. Nutrition Journal 2010, 9, 65-65, 10.1186/1475-2891-9-65.
  2. Shelby E. Bollen; Philip J. Atherton; Myogenic, genomic and non‐genomic influences of the vitamin D axis in skeletal muscle. Cell Biochemistry and Function 2020, 39, 48-59, 10.1002/cbf.3595.
  3. Joan M. Lappe; The Role of Vitamin D in Human Health: A Paradigm Shift. Journal of Evidence-Based Complementary & Alternative Medicine 2011, 16, 58-72, 10.1177/1533210110392952.
  4. Christine M. Latham; Camille R. Brightwell; Alexander R. Keeble; Brooke D. Munson; Nicholas T. Thomas; Alyaa M. Zagzoog; Christopher S. Fry; Jean L. Fry; Vitamin D Promotes Skeletal Muscle Regeneration and Mitochondrial Health. Frontiers in physiology 2021, 12, 660498, 10.3389/fphys.2021.660498.
  5. Michael F. Holick; Vitamin D Deficiency. The New England Journal of Medicine 2007, 357, 266-281, 10.1056/nejmra070553.
  6. Adriana S. Dusso; Alex J. Brown; Eduardo Slatopolsky; Vitamin D. American Journal of Physiology-Renal Physiology 2005, 289, F8-F28, 10.1152/ajprenal.00336.2004.
  7. Hector F. DeLuca; The Metabolism and Functions of Vitamin D. null 1986, 196, 361-375, 10.1007/978-1-4684-5101-6_24.
  8. Armin Zittermann; Jan F. Gummert; Nonclassical Vitamin D Actions. Nutrients 2010, 2, 408-425, 10.3390/nu2040408.
  9. Lisa Ceglia; Vitamin D and its role in skeletal muscle. Current Opinion in Clinical Nutrition and Metabolic Care 2009, 12, 628-633, 10.1097/mco.0b013e328331c707.
  10. Yu Xin Wang; Michael A. Rudnicki; Satellite cells, the engines of muscle repair. Nature Reviews Molecular Cell Biology 2011, 13, 127-133, 10.1038/nrm3265.
  11. William Chen; David Datzkiw; Michael A. Rudnicki; Satellite cells in ageing: use it or lose it. Open biology 2020, 10, 200048, 10.1098/rsob.200048.
  12. Norio Motohashi; Molecular Regulation of Muscle Satellite Cell Self-Renewal. Journal of stem cell research & therapy 2012, 01, e002, 10.4172/2157-7633.s11-e002.
  13. Nicolas A. Dumont; Yu Xin Wang; Michael A. Rudnicki; Intrinsic and extrinsic mechanisms regulating satellite cell function. Development 2015, 142, 1572-1581, 10.1242/dev.114223.
  14. Andreas Marg; Helena Escobar; Sina Gloy; Markus Kufeld; Joseph Zacher; Andreas Spuler; Carmen Birchmeier; Zsuzsanna Izsvak; Simone Spuler; Human satellite cells have regenerative capacity and are genetically manipulable. JCI Insight 2014, 124, 4257-4265, 10.1172/jci63992.
  15. Camila F. Almeida; Stephanie A. Fernandes; Antonio F. Ribeiro Junior; Oswaldo Keith Okamoto; Mariz Vainzof; Muscle Satellite Cells: Exploring the Basic Biology to Rule Them. Stem Cells International 2016, 2016, 1-14, 10.1155/2016/1078686.
  16. Karl Olsson; Amarjit Saini; Anna Strömberg; Seher Alam; Mats Lilja; Eric Rullman; Thomas Gustafsson; Evidence for Vitamin D Receptor Expression and Direct Effects of 1α,25(OH)2D3 in Human Skeletal Muscle Precursor Cells. Endocrinology 2016, 157, 98-111, 10.1210/en.2015-1685.
  17. Melissa Braga; Zena Simmons; Keith C Norris; Monica G Ferrini; Jorge N Artaza; Vitamin D induces myogenic differentiation in skeletal muscle derived stem cells. Endocrine connections 2017, 6, 139-150, 10.1530/ec-17-0008.
  18. Ratchakrit Srikuea; Muthita Hirunsai; Narattaphol Charoenphandhu; Regulation of vitamin D system in skeletal muscle and resident myogenic stem cell during development, maturation, and ageing. Scientific Reports 2020, 10, 1-17, 10.1038/s41598-020-65067-0.
  19. Kathryn H. Alliband; Sofia V. Kozhevnikova; Tim Parr; Preeti H. Jethwa; John M. Brameld; In vitro Effects of Biologically Active Vitamin D on Myogenesis: A Systematic Review. Frontiers in physiology 2021, 12, 736708, 10.3389/fphys.2021.736708.
  20. D.D.W. Cornelison; Context matters: In vivo and in vitro influences on muscle satellite cell activity. Journal of Cellular Biochemistry 2008, 105, 663-669, 10.1002/jcb.21892.
  21. Hang Yin; Feodor Price; Michael Rudnicki; Satellite Cells and the Muscle Stem Cell Niche. Physiological reviews 2013, 93, 23-67, 10.1152/physrev.00043.2011.
  22. Shihuan Kuang; Mark A. Gillespie; Michael A. Rudnicki; Niche Regulation of Muscle Satellite Cell Self-Renewal and Differentiation. Cell stem cell 2008, 2, 22-31, 10.1016/j.stem.2007.12.012.
  23. Benjamin D. Cosgrove; Alessandra Sacco; Penney M. Gilbert; Helen M. Blau; A home away from home: Challenges and opportunities in engineering in vitro muscle satellite cell niches. Differentiation 2009, 78, 185-194, 10.1016/j.diff.2009.08.004.
  24. Teresa A Davis; Marta L Fiorotto; Regulation of muscle growth in neonates. Current Opinion in Clinical Nutrition and Metabolic Care 2009, 12, 78-85, 10.1097/mco.0b013e32831cef9f.
  25. Fuminori Kawano; Yoshiaki Takeno; Naoya Nakai; Yoko Higo; Masahiro Terada; Takashi Ohira; Ikuya Nonaka; Yoshinobu Ohira; Essential role of satellite cells in the growth of rat soleus muscle fibers. American Journal of Physiology-Cell Physiology 2008, 295, C458-C467, 10.1152/ajpcell.00497.2007.
  26. Igor Bendik; Angelika Friedel; Franz F. Roos; Peter Weber; Manfred Eggersdorfer; Vitamin D: a critical and essential micronutrient for human health. Frontiers in physiology 2014, 5, 248, 10.3389/fphys.2014.00248.
  27. K. C. Hutton; M. A. Vaughn; Gilberto Litta; B. J. Turner; J. D. Starkey; Effect of vitamin D status improvement with 25-hydroxycholecalciferol on skeletal muscle growth characteristics and satellite cell activity in broiler chickens1,2. Journal of Animal Science 2014, 92, 3291-3299, 10.2527/jas.2013-7193.
  28. Hui Zhou; Yuling Chen; Gang Lv; Yong Zhuo; Yan Lin; Bin Feng; Zhengfeng Fang; Lianqiang Che; Jian Li; Shengyu Xu; et al.De Wu Improving maternal vitamin D status promotes prenatal and postnatal skeletal muscle development of pig offspring. Nutrition 2016, 32, 1144-1152, 10.1016/j.nut.2016.03.004.
  29. M. T Thayer; J. L. Nelssen; A. J. Langemeier; J. Morton; J. M. Gonzales; S. R. Kruger; Z. Ou; A. J. Makowski; J. R. Bergstrom; The Effects of Maternal Dietary Supplementation of Cholecalciferol (Vitamin D3) and 25(OH)D3 on Sow and Progeny Performance. Kansas Agricultural Experiment Station Research Reports 2018, 4, 2, 10.4148/2378-5977.7650.
  30. Gordon Warren; Mukesh Summan; Xin Gao; Rebecca Chapman; Tracy Hulderman; Petia P. Simeonova; Mechanisms of skeletal muscle injury and repair revealed by gene expression studies in mouse models. The Journal of physiology 2007, 582, 825-841, 10.1113/jphysiol.2007.132373.
  31. Yu, S., Ren, B., Chen, H., Goltzman, D., Yan, J., & Miao, D.; 1,25-Dihydroxyvitamin D deficiency induces sarcopenia by inducing skeletal muscle cell senescence. Am J Transl Res 2021, 13, 12638–12649.
  32. Ratchakrit Srikuea; Muthita Hirunsai; Effects of intramuscular administration of 1α,25(OH)2D3 during skeletal muscle regeneration on regenerative capacity, muscular fibrosis, and angiogenesis. Journal of Applied Physiology 2016, 120, 1381-1393, 10.1152/japplphysiol.01018.2015.
  33. Tohru Hosoyama; Hiroki Iida; Minako Kawai-Takaishi; Ken Watanabe; Vitamin D Inhibits Myogenic Cell Fusion and Expression of Fusogenic Genes. Nutrients 2020, 12, 2192, 10.3390/nu12082192.
  34. Kevin J P Ryan; Zoe C T R Daniel; Lucinda J L Craggs; Tim Parr; John M Brameld; Dose-dependent effects of vitamin D on transdifferentiation of skeletal muscle cells to adipose cells. Journal of Endocrinology 2013, 217, 45-58, 10.1530/joe-12-0234.
  35. Daniel J. Owens; Adam P. Sharples; Ioanna Polydorou; Nura Alwan; Timothy Donovan; Jonathan Tang; William D. Fraser; Robert G. Cooper; James P. Morton; Claire Stewart; et al.Graeme L. Close A systems-based investigation into vitamin D and skeletal muscle repair, regeneration, and hypertrophy. American Journal of Physiology-Endocrinology and Metabolism 2015, 309, E1019-E1031, 10.1152/ajpendo.00375.2015.
  36. Maura H. Parker; The altered fate of aging satellite cells is determined by signaling and epigenetic changes. Frontiers in genetics 2015, 6, 59-59, 10.3389/fgene.2015.00059.
  37. Irina M. Conboy; Michael J. Conboy; Amy J. Wagers; Eric R. Girma; Irving L. Weissman; Thomas A. Rando; Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature 2005, 433, 760-764, 10.1038/nature03260.
  38. Carla Domingues-Faria; Audrey Chanet; Jérôme Salles; Alexandre Berry; Christophe Giraudet; Véronique Patrac; Philippe Denis; Katia Bouton; Nicolas Goncalves-Mendes; Marie-Paule Vasson; et al.Yves BoirieStéphane Walrand Vitamin D deficiency down-regulates Notch pathway contributing to skeletal muscle atrophy in old wistar rats. Nutrition & Metabolism 2014, 11, 47-47, 10.1186/1743-7075-11-47.
  39. Karl Olsson; Amarjit Saini; Anna Strömberg; Seher Alam; Mats Lilja; Eric Rullman; Thomas Gustafsson; Evidence for Vitamin D Receptor Expression and Direct Effects of 1α,25(OH)2D3 in Human Skeletal Muscle Precursor Cells. Endocrinology 2016, 157, 98-111, 10.1210/en.2015-1685.
  40. Suchitra D. Gopinath; Ashley E. Webb; Anne Brunet; Thomas A. Rando; FOXO3 Promotes Quiescence in Adult Muscle Stem Cells during the Process of Self-Renewal. Stem cell reports 2014, 2, 414-426, 10.1016/j.stemcr.2014.02.002.
  41. Y Ono; F Calhabeu; J E Morgan; T Katagiri; H Amthor; P S Zammit; BMP signalling permits population expansion by preventing premature myogenic differentiation in muscle satellite cells. Cell Death & Differentiation 2010, 18, 222-234, 10.1038/cdd.2010.95.
  42. Amalia Stantzou; Elija Schirwis; Sandra Swist; Sonia Alonso-Martin; Ioanna Polydorou; Faouzi Zarrouki; Etienne Mouisel; Cyriaque Beley; Anaïs Julien; Fabien Le Grand; et al.Luis GarciaCéline ColnotCarmen BirchmeierThomas BraunMarkus SchuelkeFrédéric RelaixHelge Amthor BMP signaling regulates satellite cell dependent postnatal muscle growth. Development 2017, 144, 2737-2747, 10.1242/dev.144089.
  43. Zipora Yablonka-Reuveni; Rony Seger; Anthony J. Rivera; Fibroblast Growth Factor Promotes Recruitment of Skeletal Muscle Satellite Cells in Young and Old Rats. Journal of Histochemistry & Cytochemistry 1999, 47, 23-42, 10.1177/002215549904700104.
  44. Joe V. Chakkalakal; Kieran M. Jones; M. Albert Basson; Andrew S. Brack; The aged niche disrupts muscle stem cell quiescence. Nature 2012, 490, 355-360, 10.1038/nature11438.
  45. Josiane Joseph; Jason D. Doles; Disease-associated metabolic alterations that impact satellite cells and muscle regeneration: perspectives and therapeutic outlook. Nutrition & Metabolism 2021, 18, 1-8, 10.1186/s12986-021-00565-0.
  46. Colleen F. McKenna; Christopher S. Fry; Altered satellite cell dynamics accompany skeletal muscle atrophy during chronic illness, disuse, and aging. Current Opinion in Clinical Nutrition and Metabolic Care 2017, 20, 447-452, 10.1097/mco.0000000000000409.
  47. Lifang Han; Gang Wang; Shaopu Zhou; Chenghao Situ; Zhiming He; Yuying Li; Yudan Qiu; Yu Huang; Aimin Xu; Michael Tim Yun Ong; et al.Huating WangJianfa ZhangZhenguo Wu Muscle satellite cells are impaired in type 2 diabetic mice by elevated extracellular adenosine. Cell reports 2022, 39, 110884, 10.1016/j.celrep.2022.110884.
  48. Yasuro Furuichi; Yuki Kawabata; Miho Aoki; Yoshitaka Mita; Nobuharu L. Fujii; Yasuko Manabe; Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions. Frontiers in Cell and Developmental Biology 2021, 9, 640399, 10.3389/fcell.2021.640399.
  49. Yasuro Furuichi; Yuki Kawabata; Miho Aoki; Yoshitaka Mita; Nobuharu L. Fujii; Yasuko Manabe; Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions. Frontiers in Cell and Developmental Biology 2021, 9, 640399, 10.3389/fcell.2021.640399.
  50. Yasuro Furuichi; Yuki Kawabata; Miho Aoki; Yoshitaka Mita; Nobuharu L. Fujii; Yasuko Manabe; Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions. Frontiers in Cell and Developmental Biology 2021, 9, 640399, 10.3389/fcell.2021.640399.
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : , , , , ,
View Times: 591
Revisions: 3 times (View History)
Update Date: 10 Nov 2022
Video Production Service