TITLE:
MRCK and Myocardial Infarction: A Prospective Perspective on Cytoskeletal Kinases in Post-Infarction Repair and Ventricular Remodeling
AUTHORS:
Yunian Ai, Wenqing Gao
KEYWORDS:
MRCK, Myocardial Infarction, Perspective, Cytoskeleton, Actomyosin, Endothelial Barrier, Fibroblast, Ventricular Remodeling
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.14 No.5,
May
29,
2026
ABSTRACT: This article is a Perspective and prospective hypothesis-generating review, rather than a systematic evidence-based review. Direct evidence linking myotonic dystrophy kinase-related Cdc42-binding kinase (MRCK) to myocardial infarction (MI) remains limited. Therefore, the purpose of this article is not to conclude that MRCK is an established therapeutic target in MI, but to propose that MRCK is a biologically plausible and underexplored regulator of post-infarction repair. MI remains a major cause of heart failure and cardiovascular death despite advances in reperfusion therapy and guideline-directed medical treatment [1] [2]. Post-infarction repair involves ischemia-reperfusion injury, microvascular dysfunction, endothelial barrier disruption, inflammatory cell recruitment, fibroblast activation, scar formation, and ventricular remodeling [3]. These processes are not only governed by inflammatory, metabolic, and neurohormonal pathways, but also by cytoskeletal remodeling and cellular mechanical forces. MRCK, a Cdc42-associated serine/threonine kinase family, regulates myosin light-chain phosphorylation, actomyosin contraction, cell polarity, migration, and junctional stability. These functions overlap with several key cellular events after MI. This Perspective discusses why MRCK has been neglected in MI research, how it differs from ROCK, and which testable hypotheses may guide future studies. We propose that MRCK may represent a mechanobiological node linking local cellular contractility to endothelial integrity, inflammatory trafficking, fibroblast-mediated scar mechanics, and ventricular remodeling.