Key result
RhoA signaling mediates cardiovascular disease and cardiac remodeling but requires further therapeutic investigation.
Why the study?
The underlying mechanisms of RhoA remain poorly understood, preventing definitive conclusions being drawn regarding its protective role in the cardiovascular system.
This review highlights the crucial roles of RhoA signaling in cardiac remodeling and its potential as a therapeutic target in cardiovascular medicine.
RhoA signaling merits targeted mechanistic studies in cardiac remodeling; leaves open its viability as a therapeutic target in cardiovascular disease.
Ras homolog gene family member A (RhoA) belongs to the Rho GTPase superfamily, which was first studied in cancers as one of the essential regulators controlling cellular function. RhoA has long attracted attention as a key molecule involved in cell signaling and gene transcription, through which it affects cellular processes. A series of studies have demonstrated that RhoA plays crucial roles under both physiological states and pathological conditions in cardiovascular diseases. RhoA has been identified as an important regulator in cardiac remodeling by regulating actin stress fiber dynamics and cytoskeleton formation. However, its underlying mechanisms remain poorly understood, preventing definitive conclusions being drawn about its protective role in the cardiovascular system. In this review, we outline the characteristics of RhoA and its related signaling molecules, and present an overview of RhoA classical function and the corresponding cellular responses of RhoA under physiological and pathological conditions. Overall, we provide an update on the novel signaling under RhoA in the cardiovascular system and its potential clinical and therapeutic targets in cardiovascular medicine.
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Soh et al. (2023) conducted a review in Cardiovascular diseases. RhoA signaling was evaluated. RhoA signaling plays crucial roles in cardiovascular diseases and cardiac remodeling, though its underlying mechanisms and therapeutic potential require further investigation.
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