Sex matters in the aging heart: implications for antifibrotic therapies

Editorial FocusSex matters in the aging heart: implications for antifibrotic therapiesAlexandra M. Garvin and Taben M. HaleAlexandra M. GarvinDepartment of Basic Medical Sciences, College of Medicine-Phoenix, University of Arizona, Phoenix, Arizona and Taben M. HaleDepartment of Basic Medical Sciences, College of Medicine-Phoenix, University of Arizona, Phoenix, ArizonaPublished Online:25 Jul 2022https://doi.org/10.1152/ajpheart.00340.2022This is the final version - click for previous versionMoreSectionsFull TextPDF (227 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat "Sex matters in the aging heart: implications for antifibrotic therapies." American Journal of Physiology-Heart and Circulatory Physiology, 323(2), pp. H360–H361REFERENCES1. Angelini A, Ortiz-Urbina J, Trial J, Reddy AK, Malovannaya A, Jain A, Entman ML, Taffet GE, Cieslik KA. Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis. Am J Physiol Heart Circ Physiol 323: H285–H300, 2022. doi:10.1152/ajpheart.00078.2022.Link | ISI | Google Scholar2. Ruppert M, Barta BA, Korkmaz-Icöz S, Loganathan S, Oláh A, Sayour AA, Benke K, Nagy D, Bálint T, Karck M, Schilling O, Merkely BP, Radovits T, Szabó G. Sex similarities and differences in the reverse and anti-remodeling effect of pressure unloading therapy in a rat model of aortic banding and debanding. Am J Physiol Heart Circ Physiol 323: H204–H222, 2022. doi:10.1152/ajpheart.00654.2021.Link | Google Scholar3. Dworatzek E, Baczko I, Kararigas G. Effects of aging on cardiac extracellular matrix in men and women. Proteomics Clin Appl 10: 84–91, 2016. doi:10.1002/prca.201500031.Crossref | PubMed | ISI | Google Scholar4. Rodgers UR, Kevorkian L, Surridge AK, Waters JG, Swingler TE, Culley K, Illman S, Lohi J, Parker AE, Clark IM. Expression and function of matrix metalloproteinase (MMP)-28. Matrix Biol 28: 263–272, 2009. doi:10.1016/j.matbio.2009.04.006. Crossref | PubMed | ISI | Google Scholar5. Ma Y, Halade GV, Zhang J, Ramirez TA, Levin D, Voorhees A, Jin Y-F, Han H-C, Manicone AM, Lindsey ML. Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation. Circ Res 112: 675–688, 2013. doi:10.1161/CIRCRESAHA.111.300502. Crossref | PubMed | ISI | Google Scholar6. Cieslik KA, Taffet GE, Crawford JR, Trial J, Mejia Osuna P, Entman ML. AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction. J Mol Cell Cardiol 63: 26–36, 2013. doi:10.1016/j.yjmcc.2013.07.005. Crossref | PubMed | ISI | Google Scholar7. Garvin AM, De Both MD, Talboom JS, Lindsey ML, Huentelman MJ, Hale TM. Transient ACE (angiotensin-converting enzyme) inhibition suppresses future fibrogenic capacity and heterogeneity of cardiac fibroblast subpopulations. Hypertension 77: 904–918, 2021. doi:10.1161/HYPERTENSIONAHA.120.16352. Crossref | PubMed | ISI | Google Scholar8. Wan Q, Liu F, Zhang J, Chen H, Yan L, Li X, Sun Y, Wang J. Overexpression of laminin α4 facilitates proliferation and migration of fibroblasts in knee arthrofibrosis by targeting canonical Shh/Gli1 signaling. Connect Tissue Res 62: 464–474, 2021. doi:10.1080/03008207.2020.1773451. Crossref | PubMed | ISI | Google Scholar9. Taylor R, Long J, Yoon JW, Childs R, Sylvestersen KB, Nielsen ML, Leong KF, Iannaccone S, Walterhouse DO, Robbins DJ, Iannaccone P. Regulation of GLI1 by cis DNA elements and epigenetic marks. DNA Repair (Amst) 79: 10–21, 2019. doi:10.1016/j.dnarep.2019.04.011. Crossref | PubMed | ISI | Google Scholar10. Garvin AM, Hale TM. State of change: epigenetic and mitochondrial regulation of cardiac fibroblast activation. Curr Opin Physiol 28: 100557, 2022. doi:10.1016/j.cophys.2022.100557.Crossref | ISI | Google Scholar Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation CollectionsAJP-Heart CollectionsConsidering Sex as a Biological Variable in Cardiovascular Research Related ArticlesSex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis 11 Jul 2022American Journal of Physiology-Heart and Circulatory Physiology More from this issue > Volume 323Issue 2August 2022Pages H360-H361 Crossmark Copyright & PermissionsCopyright © 2022 the American Physiological Society.https://doi.org/10.1152/ajpheart.00340.2022PubMed35839153History Received 7 July 2022 Accepted 8 July 2022 Published online 25 July 2022 Published in print 1 August 2022 Keywordsagingcardiac fibrosisextracellular matrixfibroblastsex differences Metrics