MST1 Kinase-Cx43-YAP/TAZ Pathway Mediates Disturbed Flow Endothelial Dysfunction

老年学 医学 图书馆学 计算机科学
作者
Himanshu Meghwani,Bradford C. Berk
出处
期刊:Circulation Research [Ovid Technologies (Wolters Kluwer)]
卷期号:131 (9): 765-767 被引量:2
标识
DOI:10.1161/circresaha.122.321921
摘要

HomeCirculation ResearchVol. 131, No. 9MST1 Kinase-Cx43-YAP/TAZ Pathway Mediates Disturbed Flow Endothelial Dysfunction No AccessEditorialRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessEditorialRequest AccessFull TextMST1 Kinase-Cx43-YAP/TAZ Pathway Mediates Disturbed Flow Endothelial Dysfunction Himanshu Meghwani and Bradford C. Berk Himanshu MeghwaniHimanshu Meghwani Department of Medicine, Aab Cardiovascular Research Institute (H.M.), University of Rochester School of Medicine and Dentistry, Rochester, NY. University of Rochester Neurorestoration Institute (H.M., B.C.B.), University of Rochester School of Medicine and Dentistry, Rochester, NY. Search for more papers by this author and Bradford C. BerkBradford C. Berk Correspondence to: Bradford C. Berk, MD, PhD, University of Rochester Neurorestoration Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box URNI Rochester, NY 14642. Email E-mail Address: [email protected] https://orcid.org/0000-0002-2767-4115 University of Rochester Neurorestoration Institute (H.M., B.C.B.), University of Rochester School of Medicine and Dentistry, Rochester, NY. Search for more papers by this author Originally published13 Oct 2022https://doi.org/10.1161/CIRCRESAHA.122.321921Circulation Research. 2022;131:765–767This article is a commentary on the followingMST1 Suppresses Disturbed Flow Induced AtherosclerosisFootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Sources of Funding and Disclosures, see page 767.Correspondence to: Bradford C. Berk, MD, PhD, University of Rochester Neurorestoration Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box URNI Rochester, NY 14642. Email [email protected]rochester.eduReferences1. Humphrey JD, Schwartz MA. Vascular mechanobiology: homeostasis, adaptation, and disease.Annu Rev Biomed Eng. 2021; 23:1–27. doi: 10.1146/annurev-bioeng-092419-060810CrossrefMedlineGoogle Scholar2. Quan M, Lv H, Liu Z, Li K, Zhang C, Shi L, Yang X, Lei P, Zhu Y, Ai D. Mammalian sterile 20-like kinase 1 suppresses disturbed flow induced endothelial dysfunction and atherosclerosis.CircRes. 2022; 131:748–764. doi: 10.1161/CIRCRESAHA.122.321322LinkGoogle Scholar3. Wang K-C, Yeh Y-T, Nguyen P, Limqueco E, Lopez J, Thorossian S, Guan K-L, Li Y-SJ, Chien S. Flow-dependent YAP/TAZ activities regulate endothelial phenotypes and atherosclerosis.Proc Natl Acad Sci USA. 2016; 113:11525–11530. doi: 10.1073/pnas.1613121113.CrossrefMedlineGoogle Scholar4. Wang L, Luo J-Y, Li B, Tian XY, Chen L-J, Huang Y, Liu J, Deng D, Lau CW, Wan SA. Integrin-YAP/TAZ-JNK cascade mediates atheroprotective effect of unidirectional shear flow.Nature. 2016; 540:579–582. doi: 10.1038/nature20602CrossrefMedlineGoogle Scholar5. Niu N, Xu S, Xu Y, Little PJ, Jin Z-. g. Targeting mechanosensitive transcription factors in atherosclerosis.Trends Pharmacol Sci. 2019; 40:253–266. doi: 10.1016/j.tips.2019.02.004CrossrefMedlineGoogle Scholar6. Hao Y, Chun A, Cheung K, Rashidi B, Yang X. Tumor suppressor LATS1 is a negative regulator of oncogene YAP.J Biol Chem. 2008; 283:5496–5509. doi: 10.1074/jbc.M709037200CrossrefMedlineGoogle Scholar7. Cai X, Wang KC, Meng Z. Mechanoregulation of YAP and TAZ in Cellular Homeostasis and Disease Progression.Front Cell Dev Biol. 2021; 9:673599. doi: 10.3389/fcell.2021.673599CrossrefMedlineGoogle Scholar8. Hautefort A, Pfenniger A, Kwak BR. Endothelial connexins in vascular function.Vasc Biol. 2019; 1:H117–H124. doi: 10.1530/VB-19-0015CrossrefMedlineGoogle Scholar9. Li L, Wang M, Ma Q, Ye J, Sun G. Role of glycolysis in the development of atherosclerosis.Am J Physiol Cell Physiol. 2022; 323:C617–C629. doi: 10.1152/ajpcell.00218.2022CrossrefMedlineGoogle Scholar10. Li X, Sun X, Carmeliet P. Hallmarks of endothelial cell metabolism in health and disease.Cell Metab. 2019; 30:414–433. doi: 10.1016/j.cmet.2019.08.011CrossrefMedlineGoogle Scholar11. Ellinsworth DC, Sandow SL, Shukla N, Liu Y, Jeremy JY, Gutterman DD. Endothelium-derived hyperpolarization and coronary vasodilation: diverse and integrated roles of epoxyeicosatrienoic acids, hydrogen peroxide, and gap junctions.Microcirculation. 2016; 23:15–32. doi: 10.1111/micc.12255CrossrefMedlineGoogle Scholar12. Pfenniger A, Wong C, Sutter E, Cuhlmann S, Dunoyer-Geindre S, Mach F, Horrevoets AJ, Evans PC, Krams R, Kwak BR. Shear stress modulates the expression of the atheroprotective protein Cx37 in endothelial cells.J Mol Cell Cardiol. 2012; 53:299–309. doi: 10.1016/j.yjmcc.2012.05.011CrossrefMedlineGoogle Scholar13. Chadjichristos CE, Morel S, Derouette JP, Sutter E, Roth I, Brisset AC, Bochaton-Piallat ML, Kwak BR. Targeting connexin 43 prevents platelet-derived growth factor-BB-induced phenotypic change in porcine coronary artery smooth muscle cells.Circ Res. 2008; 102:653–660. doi: 10.1161/CIRCRESAHA.107.170472LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Yang Z, Liu R, Han X, Qiu C, Dong G, Liu Z, Liu L, Luo Y and Jiang L (2023) Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis, Molecular Medicine Reports, 10.3892/mmr.2023.12977, 27:4 Related articlesMST1 Suppresses Disturbed Flow Induced AtherosclerosisMeixi Quan, et al. Circulation Research. 2022;131:748-764 October 14, 2022Vol 131, Issue 9 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.122.321921PMID: 36252051 Originally publishedOctober 13, 2022 KeywordsEditorialsendothelial cellsgap junctionatherosclerosisconnexinPDF download Advertisement SubjectsAtherosclerosisEchocardiographyMagnetic Resonance Imaging (MRI)Nuclear Cardiology and PETTransplantation
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