Key result
Sprr3 deletion in mice preserves cardiac function and reduces fibrosis by limiting fibroblast proliferation.
Why the study?
Increased fibrosis contributes to functional decline leading to heart failure, but the role of mechanosensitive SPRR3 in cardiac fibroblasts remained unknown.
Population
Mice with pressure-induced heart failure and isolated cardiac fibroblasts
Comparison
Sprr3 deletion vs intact SPRR3 expression
Design
Preclinical in vivo and in vitro mechanistic study
Authors
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SPRR3 targeting merits investigation in fibrotic HF; animal data leave open human translation.
SPRR3 deletion preserves cardiac function and reduces fibrosis in pressure-induced heart failure by disrupting PDGFRβ and integrin β1 crosstalk in cardiac fibroblasts.
Saraswati et al. (2020) studied Heart failure and cardiac fibrosis. Sprr3 deletion was evaluated on Cardiac function and interstitial fibrosis. Sprr3 deletion in mice preserved cardiac function and reduced interstitial fibrosis in vivo, and reduced fibroblast proliferation and collagen expression in vitro.
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