Identifies p53-dependent cell cycle control as a key mechanism regulating cardiac fibrosis in left ventricular pressure overload.
p53 cell cycle control remains preclinical in overload models; leaves open whether targeting alters human fibrosis or remodeling.
This study reveals a mechanism regulating cardiac fibroblast accumulation and ECM secretion, orchestrated in part by p53-dependent cell cycle control that governs the timing and extent of fibrosis in left ventricular pressure overload.
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Liu et al. (2023) studied this question.
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