PHB2 Governs Metabolism and Phenotypic Switching of VSMCs in Vascular Remodeling

中国 表型 生物 图书馆学 医学 政治学 遗传学 法学 基因 计算机科学
作者
Kathy O. Lui,Yu Huang
出处
期刊:Circulation Research [Ovid Technologies (Wolters Kluwer)]
卷期号:131 (10): 825-827
标识
DOI:10.1161/circresaha.122.321985
摘要

HomeCirculation ResearchVol. 131, No. 10PHB2 Governs Metabolism and Phenotypic Switching of VSMCs in Vascular Remodeling No AccessEditorialRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessEditorialRequest AccessFull TextPHB2 Governs Metabolism and Phenotypic Switching of VSMCs in Vascular Remodeling Kathy O. Lui and Yu Huang Kathy O. LuiKathy O. Lui Correspondence to: Kathy O. Lui, DPhil, Department of Chemical Pathology, and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China. Email E-mail Address: [email protected] https://orcid.org/0000-0002-1616-3643 Department of Chemical Pathology, and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China (K.O.L.). Search for more papers by this author and Yu HuangYu Huang https://orcid.org/0000-0002-1277-6784 Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China (Y.H.). Search for more papers by this author Originally published27 Oct 2022https://doi.org/10.1161/CIRCRESAHA.122.321985Circulation Research. 2022;131:825–827This article is a commentary on the followingPHB2 Maintains the Contractile Phenotype of VSMCs by Counteracting PKM2 SplicingFootnotesThe 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 826 & 827.Correspondence to: Kathy O. Lui, DPhil, Department of Chemical Pathology, and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China. Email [email protected]edu.hkReferences1. Bentzon JF, Majesky MW. Lineage tracking of origin and fate of smooth muscle cells in atherosclerosis.Cardiovasc Res. 2018; 114:492–500. doi: 10.1093/cvr/cvx251CrossrefMedlineGoogle Scholar2. LeMaire SA, Russell L. Epidemiology of thoracic aortic dissection.Nat Rev Cardiol. 2011; 8:103–113. doi: 10.1038/nrcardio.2010.187CrossrefMedlineGoogle Scholar3. Li Y, Zhu H, Zhang Q, Han X, Zhang Z, Shen L, Wang L, Lui KO, He B, Zhou B. Smooth muscle-derived macrophage-like cells contribute to multiple cell lineages in the atherosclerotic plaque.Cell Discov. 2021; 7:111. doi: 10.1038/s41421-021-00328-4CrossrefMedlineGoogle Scholar4. Munshaw S, Bruche S, Redpath AN, Jones A, Patel J, Dube KN, Lee R, Hester SS, Davies R, Neal G, et al. Thymosin beta4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.J Clin Invest. 2021; doi: 10.1172/JCI127884CrossrefMedlineGoogle Scholar5. Bochaton-Piallat ML, Back M. Novel concepts for the role of smooth muscle cells in vascular disease: towards a new smooth muscle cell classification.Cardiovasc Res. 2018; 114:477–480. doi: 10.1093/cvr/cvy031CrossrefMedlineGoogle Scholar6. Shi J, Yang Y, Cheng A, Xu G, He F. Metabolism of vascular smooth muscle cells in vascular diseases.Am J Physiol Heart Circ Physiol. 2020; 319:H613–H631. doi: 10.1152/ajpheart.00220.2020CrossrefMedlineGoogle Scholar7. Patel MS, Nemeria NS, Furey W, Jordan F. The pyruvate dehydrogenase complexes: structure-based function and regulation.J Biol Chem. 2014; 289:16615–16623. doi: 10.1074/jbc.R114.563148CrossrefMedlineGoogle Scholar8. Fantin VR, St-Pierre J, Leder P. Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance.Cancer Cell. 2006; 9:425–434. doi: 10.1016/j.ccr.2006.04.023CrossrefMedlineGoogle Scholar9. Yang L, Gao L, Nickel T, Yang J, Zhou J, Gilbertsen A, Geng Z, Johnson C, Young B, Henke C, et al. Lactate promotes synthetic phenotype in vascular smooth muscle cells.Circ Res. 2017; 121:1251–1262. doi: 10.1161/CIRCRESAHA.117.311819LinkGoogle Scholar10. Chen M, Zhang J, Manley JL. Turning on a fuel switch of cancer: hnRNP proteins regulate alternative splicing of pyruvate kinase mRNA.Cancer Res. 2010; 70:8977–8980. doi: 10.1158/0008-5472.CAN-10-2513CrossrefMedlineGoogle Scholar11. Jain M, Dhanesha N, Doddapattar P, Nayak MK, Guo L, Cornelissen A, Lentz SR, Finn AV, Chauhan AK. Smooth muscle cell-specific PKM2 (Pyruvate Kinase Muscle 2) promotes smooth muscle cell phenotypic switching and neointimal hyperplasia.Arterioscler Thromb Vasc Biol. 2021; 41:1724–1737. doi: 10.1161/ATVBAHA.121.316021LinkGoogle Scholar12. Jia Y, Mao C, Ma Z, Huang J, Li W, Ma X, Zhang S, Li M, Yu F, Sun Y, et al. PHB2 maintains the contractile phenotype of VSMCs by counteracting PKM2 splicing.Circ Res. 2022; 131:807–824. doi: 10.1161/CIRCRESAHA.122.321005LinkGoogle Scholar13. David CJ, Chen M, Assanah M, Canoll P, Manley JL. HnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer.Nature. 2010; 463:364–368. doi: 10.1038/nature08697CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesPHB2 Maintains the Contractile Phenotype of VSMCs by Counteracting PKM2 SplicingYiting Jia, et al. Circulation Research. 2022;131:807-824 October 28, 2022Vol 131, Issue 10 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.122.321985PMID: 36302054 Originally publishedOctober 27, 2022 PDF download Advertisement
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