Recent advances in the role of RhoA signaling in the heart.

Authors

Shigeki Miyamoto

Published in

Journal of molecular and cellular cardiology. Oct 06, 2026. Epub Oct 06, 2026.

Abstract

Ras homolog family member A (RhoA) was originally discovered as a key regulator of cell cytoskeleton dynamics. Since then RhoA signaling research has expanded and it is now recognized that RhoA functions as a signaling hub that regulates diverse cellular functions, including cell growth, proliferation, and survival, both transcriptionally and post-transcriptionally. RhoA is activated in response to various stimuli such as G-protein coupled receptors (GPCRs), stretch and oxidative stress, and engages multiple downstream effectors. Rho-associated coiled-coil containing protein kinase (ROCK) is the first discovered effector of RhoA and other effectors include mammalian homolog of Diaphanous (mDia), phospholipase-Cε (PLCε), myocardin related transcription factor A (MRTF-A) and Yes-associated Protein (YAP). The role of RhoA in the heart has been extensively studied in last decades. Initially, studies using ROCK inhibitors suggested that activation of RhoA-ROCK signaling is deleterious in the heart, but recent studies have unveiled that RhoA in cardiomyocytes enhances fibrosis but confers cardioprotection against ischemic and non-ischemic stress through various mechanisms, including regulation of mitochondrial quality control. This review summarizes the recent progress of research on the role of RhoA signaling in the heart.

PMID:
42838442
Bibliographic data and abstract were imported from PubMed on 07 Oct 2026.

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