期刊
JOURNAL OF THE AMERICAN HEART ASSOCIATION
卷 10, 期 5, 页码 -出版社
WILEY
DOI: 10.1161/JAHA.120.019338
关键词
arrhythmias; cardiac fibroblasts; cardiomyocytes; fibrosis; heart failure; myofibroblast
资金
- British Heart Foundation [PG/17/55/33087, RG/17/15/33106, FS/19/12/34204, FS/19/16/34169, SP/15/9/31605, PG/14/59/31000, RG/14/1/30588, RM/13/30157, P47352/CRM, FS/12/40/29712]
- Wellcome Trust [109604/Z/15/Z, 201543/B/16/Z]
- Animal Free Research UK [AFR19-20293]
- National Centre for the Replacement, Refinement, and Reduction of Animals in Research [CRACK-IT:35911-259146, NC/K000225/1, NC/T001747/1]
- Accelerator Award [AA/18/2/34218]
- Oxford British Heart Foundation Centre of Research Excellence [RE/13/1/30181]
- Wellcome Trust [109604/Z/15/Z] Funding Source: Wellcome Trust
Cardiac fibroblasts play a crucial role in providing support to the heart and are involved in physiological signaling processes, but excessive activation can lead to pathological remodeling. Research is expanding our understanding of cardiac fibroblast activation and their interactions with cardiac myocytes.
Cardiac fibroblasts are the primary cell type responsible for deposition of extracellular matrix in the heart, providing support to the contracting myocardium and contributing to a myriad of physiological signaling processes. Despite the importance of fibrosis in processes of wound healing, excessive fibroblast proliferation and activation can lead to pathological remodeling, driving heart failure and the onset of arrhythmias. Our understanding of the mechanisms driving the cardiac fibroblast activation and proliferation is expanding, and evidence for their direct and indirect effects on cardiac myocyte function is accumulating. In this review, we focus on the importance of the fibroblast-to-myofibroblast transition and the cross talk of cardiac fibroblasts with cardiac myocytes. We also consider the current use of models used to explore these questions.
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