Key result
Belumosudil, a ROCK2-specific inhibitor, effectively ameliorated cardiac hypertrophy, fibrosis, and dysfunction induced by transverse aortic constriction by inhibiting cardiac fibroblast activation.
Why the study?
Although ROCK2 is the main ROCK isoform in the heart and key in cardiac hypertrophy and fibrosis, there has been no selective pharmacological approach to inhibit ROCK2.
Does belumosudil ameliorate cardiac hypertrophy, fibrosis, and dysfunction in TAC-induced models?
Does belumosudil ameliorate cardiac hypertrophy, fibrosis, and dysfunction in TAC-induced models?
Belumosudil, a ROCK2-specific inhibitor, shows promise in ameliorating cardiac hypertrophy and fibrosis in preclinical models.
Cautious interpretation required for this animal study; leaves open translation of ROCK2 inhibition to human heart failure therapy.
Although ρ-associated kinase-2 (ROCK2) is the main isoform of ρ-associated kinases (ROCKs) in the heart and more important in cardiac hypertrophy and fibrosis than ρ-associated kinase-1 (ROCK1), there has not been any pharmacological approach to inhibit ROCK2 selectively. Our study demonstrates for the first time that belumosudil, the first ROCK2-specific inhibitor, effectively ameliorates cardiac hypertrophy, fibrosis, and dysfunction induced by TAC via inhibiting cardiac fibroblasts activation.
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Liu et al. (2022) studied Cardiac hypertrophy and fibrosis. Belumosudil was evaluated on Cardiac hypertrophy, fibrosis, and dysfunction induced by TAC. Belumosudil, a ROCK2-specific inhibitor, effectively ameliorated cardiac hypertrophy, fibrosis, and dysfunction induced by transverse aortic constriction by inhibiting cardiac fibroblast activation.
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