ReviewCell biochemistry and function2026
Research Progress on the ARHGEF Family in Cardiovascular Diseases.
Review in Cell biochemistry and function, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
The ARHGEF (Rho guanine nucleotide exchange factor) family acts as a key upstream regulator of Rho GTPases, including RhoA, Rac1, and Cdc42. It plays critical roles in cytoskeletal remodeling, cell migration, vascular tone regulation, and inflammatory responses. Recent studies have shown that dysregulated ARHGEF activity contributes to cardiovascular diseases such as atherosclerosis, hypertension, cardiac hypertrophy, fibrosis, and myocardial ischemia/reperfusion injury. However, the functions of ARHGEFs in specific cell types and their overall signaling mechanisms in the cardiovascular system remain poorly understood. This review provides a comprehensive framework of current progress in understanding the molecular mechanisms underlying ARHGEF-mediated regulation in endothelial dysfunction, vascular remodeling, myocardial fibrosis, and ischemia/reperfusion injury. It also highlights potential pharmacological strategies that target the ARHGEF and Rho GTPase signaling axis for precise therapeutic intervention. By integrating molecular, cellular, and translational research, this work offers a conceptual framework for ARHGEF-driven signaling in cardiovascular diseases, and offers new insights for future drug development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.