SerpinA3 is an endogenous TGF-β receptor antagonist that attenuates cardiac fibroblast activation and fibrotic remodeling

Pharmacological supplementation or genetic augmentation of SerpinA3 markedly attenuated cardiac dysfunction and fibrotic remodeling in response to pressure overload. Single-cell transcriptomic analyses further demonstrated that SerpinA3 suppresses profibrotic fibroblast programs by promoting a transition from activated and extracellular matrix–producing fibroblasts toward a quiescent, pro-angiogenesis state.