Your browser does not fully support modern features. Please upgrade for a smoother experience.
Connexome-Associated Pathways in Atherosclerosis: Comparison
View Latest Version
Please note this is a comparison between Version 2 by Jose Francisco Islas and Version 1 by Jose Francisco Islas.

The connexome comprises the network of intercellular communication structures formed by connexins, pannexins, and associated regulatory proteins within the vasculature. These channels enable the exchange of ions, metabolites, and signaling molecules between endothelial cells, vascular smooth muscle cells, immune cells, and fibroblasts. In healthy vessels, the connexome maintains endothelial quiescence, shear stress responsiveness, and coordinated vascular homeostasis. In atherosclerosis, disturbed flow, inflammation, and oxidative stress remodel connexome composition—most notably through increased Cx43 expression, reduced Cx37/Cx40 activity, and enhanced Panx1-mediated ATP release. These alterations promote endothelial activation, leukocyte recruitment, smooth muscle proliferation, and inflammasome signaling, positioning the connexome as a central regulator of vascular dysfunction and plaque progression.

  • connexome
  • krupple-like factors

# Connexome-Associated Pathways in AtherosclerosisConnexome-Associated Pathways in Atherosclerosis

 Overview

## Overview

The connexome refers to the coordinated network of connexins (Cx), pannexins (Panx), gap junctions (GJ), hemichannels, and interacting proteins that mediate electrical, metabolic, and paracrine communication among the vascular cells. This communication is essential for maintaining endothelial integrity, vascular tone, inflammatory balance, and smooth muscle phenotype. AUnfortunetlly, the development of atherosclerosis profoundly disturbs these communication systems, leading to endothelial dysfunction, leukocyte recruitment, maladaptive smooth muscle remodeling, chronic inflammation, and ultimately plaque destabilization (1, 2, 14)[1][2][3]. Regions of disturbed flow exhibit marked upregulation of pro-atherogenic connexins—particularly connexin 43 (Cx43)—which amplifies ATP release, immune activation, and endothelial permeability (7, 15, 19, 21)[4][5][6][7].

 Connexome Components

## Connexome Components

Connexins form hexameric hemichannels that pair to create gap junctions enabling direct cytoplasmic component exchange. Amongst these connexins, Connexin 37 (Cx37) is enriched in the arterial endothelium and plays a protective role by limiting monocyte adhesion and supporting endothelial quiescence (15, 28)[5][8]. Connexin 40 (Cx40) promotes nitric oxide production, maintains anti-inflammatory signaling, and supports vascular homeostasis (28, 46)[8][9]. In contrast, connexin 43 (Cx43) is strongly induced under oscillatory shear stress and inflammatory conditions (7[4][5][7], 15, 21), where it promotes leukocyte adhesion, macrophage infiltration, foam cell formation, and smooth muscle migration (18, 30)[10][11]. Connexin 45 (Cx45) participates in vascular development and smooth muscle electrical communication (35)[12].

 

On the other hand, Pannexins and particular Pannexin 1 (Panx1) functions predominantly as a mechanosensitive ATP-release channel activated by cytokines, oxidative stress, and mechanical strain (22, 24)[13][14]. Panx1-mediated ATP release triggers purinergic P2X7 receptor activation, K+ efflux, and NLRP3 inflammasome assembly, ecausing pyroptosis and accumulation of debris, hence escalating inflammatory signaling in atherosclerosis (22, 31)[13][15].

 Connexome Remodeling in Atherosclerosis

## Connexome Remodeling in Atherosclerosis

Atherosclerotic lesions preferentially develop in arterial branches or curvatures where blood flow is disturbed. Here, endothelial cells can lose their protective flow-dependent transcriptional programs and move toward an inflammatory phenotype characterized by reducedthe reduction of both KLF2 and KLF4 expression (28, 46, 49)[8][9][16]. This shift decreases the protective expression of both Cx37 and Cx40 expression (15, 28) [5][8] and increases the expression and phosphorylation of Cx43 (7, 18, 21)[4][10][7].

 

Enhanced ATP release through bith Cx43 and Panx1 amplifies endothelial activation and leukocyte recruitment (22, 24, 31)[13][14][15]. Smooth muscle cells respond to increased Cx43 signaling by adopting a synthetic, proliferative phenotype conducive to neointimal growth (18, 30)[10][11].

 

Panx1-dependent ATP release activates the NLRP3 inflammasome, leading to secuential caspase-1 activation and IL-1β secretion, processes that contribute to necrotic core expansion and plaque vulnerability (22, 31, 40)[13][15][17].

 Regulatory Pathways Governing the Connexome

# Regulatory Pathways Governing the Connexome1. The KLF2/KLF4 Shear-Stress Axis

 

## 1. The KLF2/KLF4 Shear-Stress Axis

Laminar shear stress activates the MEKK2–MEK5–ERK5 pathway, stimulating MEF2 and resulting in the upregulation of both KLF2 and KLF4 (28, 46, 49)[8][9][16]. These transcription factors enhance expression of both Cx37 and Cx40 (15, 28) [5][8] while suppressing Cx43 (7, 21)[4][7]. Loss of the KLF2/KLF4 signaling under disturbed flow fosters endothelial inflammation and connexome dysregulation.

 2. NF-κB Pathway

## 2. NF-κB Pathway

Inflammatory cytokines— including TNF-α and IL-1β— can help activate NF-κB signaling, which in turn increases Cx43 transcription and drives phosphorylation patterns favoring hemichannel opening (7, 21, 20)[4][7][18]. This promotes endothelial activation, barrier dysfunction, and leukocyte recruitment (1, 14)[1][3].

 3. MAPK Pathways

## 3. MAPK Pathways

ERK, JNK, and p38 MAPKs modify the overall connexin behavior through transcriptional and post-translational mechanisms. First, ERK promotes Cx43 internalization and turnover[18], (20),then JNK elevates Cx43 expression during oxidative stress (30)[11], and finally p38 increases hemichannel opening and inflammatory coupling (31)[15].

 4. PI3K–Akt/eNOS Signaling

## 4. PI3K–Akt/eNOS S signaling

Akt promotes endothelial homeostasis and supports Cx40 expression (28). Reduced nitric oxide bioavailability—, a common in condition in atherosclerosis— enhances Cx43 hemichannel opening and promotes endothelial dysfunction (35)[12].

 5. Notch Signaling

## 5. Notch Signaling

Laminar shear stimulates Notch1–RBPJ signaling, which in turn suppresses Cx43 expression and maintains endothelial quiescence[16]. (49).Meanwhile the Lloss of Notch activity in disturbed flow promotes endothelial-mesenchymal transition and enhances vascular inflammation (18)[10].

 6. TGF-β/SMAD Pathway

## 6. TGF-β/SMAD Pathway

TGF-β signaling induces Cx43 through SMAD2/3the activation (20, of SMAD2/30)[18][11]. Crosstalk with RhoA/ROCK and YAP/TAZ mechanotransduction pathways intensifies cytoskeletal tension, enhances matrix remodeling, and promotes connexin trafficking (48, 52)[19][20].

 7. Oxidative Stress & Nrf2

## 7. Oxidative Stress & Nrf2

Reactive oxygen species oxidize Cx43 and Panx1, increasing hemichannel activity and weakening endothelial integrity[15]. (31).Nontheless, Nrf2 activation counters these effects by restoring antioxidant defenses and supporting Cx37 and Cx40 expression (24)[14]. However, Nrf2 is often suppressed in plaques (31)[15].

 8. NLRP3 Inflammasome Activation

## 8. NLRP3 Inflammasome Activatioan

Panx1-mediated ATP release activates P2X7 and the NLRP3 inflammasome (22, 31)[13][15]. This leads to caspase-1 activation and IL-1β maturation, both key contributors to plaque expansion and inflammation (39, 40)[21][17].

 9. RhoA/ROCK Mechanotransduction

## 9. RhoA/ROCK Mechanotransduction

RenhoA/ROCK enhances actomyosin tension and increases the trafficking of Cx43 to the plasma membrane under disturbed flow, promoting inflammatory remodeling (48)[19].

 10. YAP/TAZ Mechanotransduction

## 10. YAP/TAZ Mechanotransduction

YAP and and TAZ both respond to changes in matrix stiffness and oscillatory shear by entering the nucleus and increasing Cx43 transcription (52). This activation promotes smooth muscle proliferation and migration, thereby contributing to the overall plaque progression (53)[13].

 Nanomedicine and Therapeutic Modulation of the Connexome

# Nanomedicine and Therapeutic Modulation of the Connexome

Nanotetechnology offers new tools for imaging, modulating, and repairing connexome signaling, which is a potentially crucial step in mitigating the developmemnt, as well as the effects of atherosclerosis. Targeted nanoparticles that bind VCAM-1, ICAM-1, macrophages, or oxidized lipids provide highly sensitive plaque imaging (37, 38, 42)[22][23][24]. Therapeutic delivery systems—including siRNA, miRNA mimics/inhibitors, and mRNA nanoparticles—are being developed to restore KLF2/KLF4 signaling or suppress Cx43 and Panx1 activation (27, 39)[25][21]. Connexin-modulating peptides such as Gap26, Gap27, and TAT-Gap19 can selectively inhibit Cx43 hemichannels when delivered via nanoparticles (47)[26]. Multifunctional theranostic platforms combine real-time imaging with connexome-targeted therapy (40, 52, 53)[17][20][27].

  

# Future DirectionsFuture Directions

Emerging technologies—including single-cell transcriptomics, spatial proteomics, and computational flow modeling—are revealing cell-specific patterns of connexome regulation in unprecedented detail (49)[16]. The integration of mechanobiology, inflammation, and nanotherapeutics is guiding next-generation strategies aimed at normalizing Cx37, Cx40, Cx43, and Panx1 activity. Precision modulation of the connexome signaling is increasingly seen as a promising approach for the stabilizing of plaques and reducing the burden of atherosclerotic cardiovascular disease (27, 52, 53)[17][20][27].

 

# References

 

  1. Tabas I, Lichtman AH. Monocyte-macrophages and T cells in atherosclerosis. *Immunity.* 2017;47:621–634.
  2. Jebari-Benslaiman S, Galicia-García U, Larrea-Sebal A, et al. Pathophysiology of atherosclerosis. *Int J Mol Sci.* 2022;23:3346.
  3. Perrotta I. The dance of atherosclerosis. *Int J Mol Sci.* 2022;23:3444.
  4. Pedro-Botet J, Climent E, Benaiges D. Atherosclerosis and inflammation. *Med Clin (Barc).* 2020;155:256–262.
  5. Jaffer FA, Verjans JW. Imaging atherosclerosis. *Heart.* 2014;100:1469–1477.
  6. Wong CW, Christen T, van der Rest B, et al. Molecular profiling of the endothelium. *Nat Med.* 2006;12:950–954.
  7. Pfenniger A, Wohlwend A, Kwak BR. Connexins and atherosclerosis. *Biochim Biophys Acta.* 2013;1828:157–166.
  8. Koval M. Gap junctions in endothelial biology. In: *Encyclopedia of Respiratory Medicine.* 2006.
  9. Tasouli-Drakou V, et al. Connexins in cardiovascular immunology. *Int J Mol Sci.* 2025;26:1364.
  10. Naiya T, et al. Connexins in cardiovascular disease. *Am J Physiol Heart Circ Physiol.* 2024.
  11. Powell-Wiley TM, et al. Obesity and atherosclerosis. *Circulation.* 2021;143.
  12. Nelson DL, Cox MN. *Lehninger Principles of Biochemistry.* W.H. Freeman; 2012.
  13. Ferrier DR. *Lippincott Illustrated Reviews: Biochemistry.* 7th ed. 2017.
  14. Susser LI, Rayner KJ. Immunometabolism in atherosclerosis. *J Clin Invest.* 2022;132.
  15. Meens MJ, et al. Connexin37 and endothelial function. *Cardiovasc Res.* 2013;99:304–314.
  16. Wu X, et al. Metabolic inflammation. *Front Immunol.* 2023;14:1225178.
  17. Denis JF, et al. Cx43 in cell differentiation. *Oncotarget.* 2017;8:50972–50986.
  18. Márquez M, et al. Connexins in vascular remodeling. *J Vasc Res.* 2023;60:87–100.
  19. Tu S, et al. Cx43 and inflammation. *Naunyn Schmiedebergs Arch Pharmacol.* 2017;390:651–660.
  20. Geimonen E, et al. Phosphorylation of Cx43. *J Biol Chem.* 1996;271:23667–23674.
  21. Kam CY, et al. Mechanobiology of Cx43. *J Cell Biol.* 2018;217:3219–3235.
  22. Yu H, et al. Panx1 in inflammasome activation. *J Neuroinflammation.* 2020;17:322.
  23. Vielma AZ, et al. Panx1 channels in disease. *Int J Mol Sci.* 2020;21:5415.
  24. Rusiecka OM, et al. Nrf2 and gap junctions. *Biomolecules.* 2020;10:1225.
  25. Li YJ, et al. Connexins in inflammation. *Biology (Basel).* 2023;12:346.
  26. Santoyo-Suarez MG, et al. Connexome in metabolic disease. *Life (Basel).* 2023;13:420.
  27. Li H, et al. Nanomedicine targeting Cx43. *Theranostics.* 2021;11:1609–1625.
  28. Boon RA, et al. Shear stress and KLF2. *Arterioscler Thromb Vasc Biol.* 2007;27:532–539.
  29. Denis JF, et al. Cx43 in physiology. *Front Physiol.* 2019;10:80.
  30. Yang H, et al. Cx43 in oxidative stress. *Biochem Biophys Res Commun.* 2018;495:2376–2382.
  31. Dabravolski SA, et al. Inflammasome and atherosclerosis. *Biomedicines.* 2022;10:254.
  32. Lucero CM, et al. Epigenetics in vascular disease. *Int J Mol Sci.* 2022;23:10097.
  33. Evans PM, et al. Wnt signaling. *Mol Cell Biol.* 2010;30:372–381.
  34. Liu H, et al. Apoptosis and Cx43. *Med Sci Monit.* 2016;22:2451–2462.
  35. Davis MJ, et al. Vascular physiology. *Physiol Rev.* 2023;103:1247–1421.
  36. Pamukcu B, et al. Platelet signaling. *Thromb Res.* 2011;128:117–123.
  37. Nahrendorf M, et al. Nanoparticle imaging. *JACC Cardiovasc Imaging.* 2009;2:1213–1222.
  38. Jayagopal A, et al. Nanotechnology in CVD. *Nanotechnology.* 2009;20:165102.
  39. Punjabi M, et al. Nanotherapy in atherosclerosis. *Arterioscler Thromb Vasc Biol.* 2019;39:2520–2530.
  40. Yan F, et al. Nanotheranostics. *Theranostics.* 2018;8:1879–1891.
  41. Seo JW, et al. Targeted nanoparticles. *Bioconjug Chem.* 2014;25:231–239.
  42. Senders ML, et al. Molecular imaging. *JACC Cardiovasc Imaging.* 2019;12:2015–2026.
  43. Lamb YN. New pharmacotherapies. *Drugs.* 2021;81:389–395.
  44. Tao W, et al. RNA nanotherapeutics. *Sci Transl Med.* 2020;12:eAAY1063.
  45. Guo Y, et al. Advanced nanomedicine. *Adv Sci.* 2022;9:2105875.
  46. Fledderus JO, et al. KLF2 regulation. *Arterioscler Thromb Vasc Biol.* 2008;28:1339–1346.
  47. Pfenniger A, et al. Cx43 inhibitors. *J Mol Cell Cardiol.* 2012;53:299–309.
  48. Okamoto T, et al. Connexin mechanotransduction. *Biochim Biophys Acta Mol Basis Dis.* 2021;1867:166168.
  49. Davies PF, et al. Shear stress landscape. *Cardiovasc Res.* 2013;99:315–327.
  50. Zhou Z, et al. Preprint (bioengineering). 2025.
  51. Cordes KR, et al. miR-145 in vascular biology. *Nature.* 2009;460:705–710.
  52. Perera B, et al. Biomaterials & mechanobiology. *Mater Today Bio.* 2023;22:100767.
  53. Zhong Z, et al. Nanomaterials in CVD. *Mater Today Bio.* 2024;29:101308.

References

  1. Ira Tabas; Andrew H. Lichtman; Monocyte-Macrophages and T Cells in Atherosclerosis. Immun.. 2017, 47, 621-634.
  2. Shifa Jebari-Benslaiman; Unai Galicia-García; Asier Larrea-Sebal; Javier Rekondo Olaetxea; Iraide Alloza; Koen Vandenbroeck; Asier Benito-Vicente; César Martín; Pathophysiology of Atherosclerosis. Int. J. Mol. Sci.. 2022, 23, 3346.
  3. Leah I. Susser; Katey J. Rayner; Through the layers: how macrophages drive atherosclerosis across the vessel wall. J. Clin. Investig.. 2022, 132, e157011.
  4. Anna Pfenniger; Marc Chanson; Brenda R. Kwak; Connexins in atherosclerosis. Biochim. et Biophys. Acta (BBA) - Biomembr.. 2013, 1828, 157-166.
  5. Merlijn J. Meens; Anna Pfenniger; Brenda R. Kwak; Mario Delmar; Regulation of cardiovascular connexins by mechanical forces and junctions. Cardiovasc. Res.. 2013, 99, 304-314.
  6. Su Tu; Fu-Tao Cao; Xiao-Chun Fan; Cheng-Jian Yang; Resveratrol protects the loss of connexin 43 induced by ethanol exposure in neonatal mouse cardiomyocytes. Naunyn-Schmiedeberg's Arch. Pharmacol.. 2017, 390, 651-660.
  7. Chen Yuan Kam; Adi D. Dubash; Elisa Magistrati; Simona Polo; Karla J.F. Satchell; Farah Sheikh; Paul D. Lampe; Kathleen J. Green; Desmoplakin maintains gap junctions by inhibiting Ras/MAPK and lysosomal degradation of connexin-43. J. Cell Biol.. 2018, 217, 3219-3235.
  8. Reinier A. Boon; Joost O. Fledderus; Oscar L. Volger; Eva J.A. van Wanrooij; Evangelia Pardali; Frank Weesie; Johan Kuiper; Hans Pannekoek; Peter Ten Dijke; Anton J.G. Horrevoets; KLF2 Suppresses TGF-β Signaling in Endothelium Through Induction of Smad7 and Inhibition of AP-1. Arter. Thromb. Vasc. Biol.. 2007, 27, 532-539.
  9. Joost O. Fledderus; Reinier A. Boon; Oscar L. Volger; Hanna Hurttila; Seppo Ylä-Herttuala; Hans Pannekoek; Anna-Liisa Levonen; Anton J.G. Horrevoets; KLF2 Primes the Antioxidant Transcription Factor Nrf2 for Activation in Endothelial Cells. Arter. Thromb. Vasc. Biol.. 2008, 28, 1339-1346.
  10. Mónica Márquez; Matías Muñoz; Alexandra Córdova; Mariela Puebla; Xavier F. Figueroa; Connexin 40-Mediated Regulation of Systemic Circulation and Arterial Blood Pressure. J. Vasc. Res.. 2023, 60, 87-100.
  11. Haojie Yang; Xixiang Xi; Bin Zhao; Zhenxi Su; Zhenyi Wang; KLF4 protects brain microvascular endothelial cells from ischemic stroke induced apoptosis by transcriptionally activating MALAT1. Biochem. Biophys. Res. Commun.. 2018, 495, 2376-2382.
  12. Michael J. Davis; Scott Earley; Yi-Shuan Li; Shu Chien; Vascular mechanotransduction. Physiol. Rev.. 2023, 103, 1247-1421.
  13. Hailong Yu; Xiang Cao; Wei Li; Pinyi Liu; Yuanyuan Zhao; Lilong Song; Jian Chen; Beilei Chen; Wenkui Yu; Yun Xu; Targeting connexin 43 provides anti-inflammatory effects after intracerebral hemorrhage injury by regulating YAP signaling. J. Neuroinflammation. 2020, 17, 1-19.
  14. Olga M. Rusiecka; Jade Montgomery; Sandrine Morel; Daniela Batista-Almeida; Raf Van Campenhout; Mathieu Vinken; Henrique Girao; Brenda R. Kwak; Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection. Biomol.. 2020, 10, 1225.
  15. Siarhei A. Dabravolski; Vasily N. Sukhorukov; Vladislav A. Kalmykov; Andrey V. Grechko; Nikolay K. Shakhpazyan; Alexander N. Orekhov; The Role of KLF2 in the Regulation of Atherosclerosis Development and Potential Use of KLF2-Targeted Therapy. Biomed.. 2022, 10, 254.
  16. Peter F. Davies; Mete Civelek; Yun Fang; Ingrid Fleming; The atherosusceptible endothelium: endothelial phenotypes in complex haemodynamic shear stress regions in vivo. Cardiovasc. Res.. 2013, 99, 315-327.
  17. Fei Yan; Yu Sun; Yang Mao; Meiying Wu; Zhiting Deng; Shuai Li; Xin Liu; Li Xue; Hairong Zheng; Ultrasound Molecular Imaging of Atherosclerosis for Early Diagnosis and Therapeutic Evaluation through Leucocyte-like Multiple Targeted Microbubbles. Theranostics. 2018, 8, 1879-1891.
  18. Erika Geimonen; Wei Jiang; Mariam Ali; Glenn I. Fishman; Robert E. Garfield; Janet Andersen; Activation of Protein Kinase C in Human Uterine Smooth Muscle Induces connexin-43 Gene Transcription through an AP-1 Site in the Promoter Sequence. J. Biol. Chem.. 1996, 271, 23667-23674.
  19. Takayuki Okamoto; Eun Jeong Park; Eiji Kawamoto; Haruki Usuda; Koichiro Wada; Akihiko Taguchi; Motomu Shimaoka; Endothelial connexin-integrin crosstalk in vascular inflammation. Biochim. et Biophys. Acta (BBA) - Mol. Basis Dis.. 2021, 1867, 166168.
  20. Binura Perera; Yuao Wu; Nam-Trung Nguyen; Hang Thu Ta; Advances in drug delivery to atherosclerosis: Investigating the efficiency of different nanomaterials employed for different type of drugs. Mater. Today Bio. 2023, 22, 100767.
  21. Mukesh Punjabi; Lifen Xu; Amanda Ochoa-Espinosa; Alexandra Kosareva; Thomas Wolff; Ahmed Murtaja; Alexis Broisat; Nick Devoogdt; Beat A. Kaufmann; Ultrasound Molecular Imaging of Atherosclerosis With Nanobodies. Arter. Thromb. Vasc. Biol.. 2019, 39, 2520-2530.
  22. Matthias Nahrendorf; Edmund Keliher; Peter Panizzi; Hanwen Zhang; Sheena Hembrador; Jose-Luiz Figueiredo; Elena Aikawa; Kimberly Kelly; Peter Libby; Ralph Weissleder; 18F-4V for PET–CT Imaging of VCAM-1 Expression in Atherosclerosis. JACC: Cardiovasc. Imaging. 2009, 2, 1213-1222.
  23. Ashwath Jayagopal; Yan Ru Su; John L Blakemore; MacRae F Linton; Sergio Fazio; Frederick R Haselton; Quantum dot mediated imaging of atherosclerosis. Nanotechnol.. 2009, 20, 165102-165102.
  24. Max L. Senders; Sophie Hernot; Giuseppe Carlucci; Jan C. van de Voort; Francois Fay; Claudia Calcagno; Jun Tang; Amr Alaarg; Yiming Zhao; Seigo Ishino; Anna Palmisano; Gilles Boeykens; Anu E. Meerwaldt; Brenda L. Sanchez-Gaytan; Samantha Baxter; Laura Zendman; Mark E. Lobatto; Nicolas A. Karakatsanis; Philip M. Robson; Alexis Broisat; Geert Raes; Jason S. Lewis; Sotirios Tsimikas; Thomas Reiner; Zahi A. Fayad; Nick Devoogdt; Willem J.M. Mulder; Carlos Pérez-Medina; Nanobody-Facilitated Multiparametric PET/MRI Phenotyping of Atherosclerosis. JACC: Cardiovasc. Imaging. 2019, 12, 2015-2026.
  25. Hongda Li; Yanfang Wang; Jiwen Liu; Xiaoli Chen; Yunhao Duan; Xiaoyu Wang; Yajing Shen; Yashu Kuang; Tao Zhuang; Brain Tomlinson; Paul Chan; Zuoren Yu; Yu Cheng; Lin Zhang; Zhongmin Liu; Yuzhen Zhang; Zhenlin Zhao; Qi Zhang; Jie Liu; Endothelial Klf2-Foxp1-TGFβ signal mediates the inhibitory effects of simvastatin on maladaptive cardiac remodeling. Theranostics. 2021, 11, 1609-1625.
  26. Anna Pfenniger; Cindy Wong; Esther Sutter; Simon Cuhlmann; Sylvie Dunoyer-Geindre; François Mach; Anton J. Horrevoets; Paul C. Evans; Rob Krams; Brenda R. Kwak; Shear stress modulates the expression of the atheroprotective protein Cx37 in endothelial cells. J. Mol. Cell. Cardiol.. 2012, 53, 299-309.
  27. Ziqiao Zhong; Lu Gan; Ziyi Feng; Wenhao Wang; Xin Pan; Chuanbin Wu; Ying Huang; Hydrogel local drug delivery systems for postsurgical management of tumors: Status Quo and perspectives. Mater. Today Bio. 2024, 29, 101308.
  28. Ziqiao Zhong; Lu Gan; Ziyi Feng; Wenhao Wang; Xin Pan; Chuanbin Wu; Ying Huang; Hydrogel local drug delivery systems for postsurgical management of tumors: Status Quo and perspectives. Mater. Today Bio. 2024, 29, 101308.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
Academic Video Service
Feedback