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Inhibiting RhoA Activation via GDP-state Stabilization to Relieve Heart Failure
Abstract High rates of heart failure (HF) morbidity and mortality have made targeting myocardial remodeling, particularly hypertrophy and fibrosis, a key therapeutic focus. RhoA, which regulates cytoskeletal reorganization and cell migration, plays a role in this process. However, RhoA has long been considered "undruggable", due to its strong binding to its endogenous substrates, GDP/GTP, and the lack of well-defined pockets for drug targeting.
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