PU.1 inhibition does not attenuate cardiac function deterioration or fibrosis in a murine model of myocardial infarction
Author:
Funder
National Institute for Health Care Management Foundation
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Clinical Biochemistry,Molecular Biology,General Medicine
Link
https://link.springer.com/content/pdf/10.1007/s11010-022-04561-7.pdf
Reference49 articles.
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3. Villalobos E, Criollo A, Schiattarella GG, Altamirano F, French KM, May HI, Jiang N, Nguyen NUN, Romero D, Roa JC, Garcia L, Diaz-Araya G, Morselli E, Ferdous A, Conway SJ, Sadek HA, Gillette TG, Lavandero S, Hill JA (2019) Fibroblast primary cilia are required for cardiac fibrosis. Circulation 139:2342–2357. https://doi.org/10.1161/CIRCULATIONAHA.117.028752
4. Kong P, Shinde AV, Su Y, Russo I, Chen B, Saxena A, Conway SJ, Graff JM, Frangogiannis NG (2018) Opposing actions of fibroblast and cardiomyocyte Smad3 signaling in the infarcted myocardium. Circulation 137:707–724. https://doi.org/10.1161/CIRCULATIONAHA.117.029622
5. Kanisicak O, Khalil H, Ivey MJ, Karch J, Maliken BD, Correll RN, Brody MJ, J Lin SC, Aronow BJ, Tallquist MD, Molkentin JD (2016) Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nat Commun 7:12260. https://doi.org/10.1038/ncomms12260
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