This review summarizes the role of various ion channels, including TRP, Piezo1, and CRAC, in myocardial fibroblast activation and cardiac fibrosis to identify potential new therapeutic targets.
Ion channels in cardiac fibroblasts play a critical role in the development of myocardial fibrosis and may serve as novel therapeutic targets to prevent heart failure.
Cardiac fibrosis is defined as excessive deposition of extracellular matrix (ECM) in pathological conditions. Cardiac fibroblasts (CFs) activated by injury or inflammation differentiate into myofibroblasts (MFs) with secretory and contractile functions. In the fibrotic heart, MFs produce ECM which is composed mainly of collagen and is initially involved in maintaining tissue integrity. However, persistent fibrosis disrupts the coordination of excitatory contractile coupling, leading to systolic and diastolic dysfunction, and ultimately heart failure. Numerous studies have demonstrated that both voltage- and non-voltage-gated ion channels alter intracellular ion levels and cellular activity, contributing to myofibroblast proliferation, contraction, and secretory function. However, an effective treatment strategy for myocardial fibrosis has not been established. Therefore, this review describes the progress made in research related to transient receptor potential (TRP) channels, Piezo1, Ca 2+ release-activated Ca 2+ (CRAC) channels, voltage-gated Ca 2+ channels (VGCCs), sodium channels, and potassium channels in myocardial fibroblasts with the aim of providing new ideas for treating myocardial fibrosis.
Xing et al. (Thu,) conducted a review in Cardiac fibrosis. Ion channels (TRP, Piezo1, CRAC, VGCCs, sodium, potassium) was evaluated. This review summarizes the role of various ion channels, including TRP, Piezo1, and CRAC, in myocardial fibroblast activation and cardiac fibrosis to identify potential new therapeutic targets.
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