Key result
Fibroblast-specific deletion of the CNP receptor GC-B in mice exacerbated cardiac fibrosis, hypertrophy, and contractile dysfunction in response to angiotensin II infusion or transverse aortic constriction, with more pronounced effects in females.
Why the study?
The local mediators that counterregulate excessive activation of cardiac fibroblasts in response to injury remain unclear, and the role of endogenous C-type natriuretic peptide is not fully known.
Population
Mice with fibroblast-restricted deletion of GC-B, and human and murine cardiac fibroblasts
Comparison
Fibroblast-specific GC-B knockout vs control mice exposed to Ang II or TAC
Design
Preclinical animal and in vitro laboratory study
Follow-up
2 weeks
Authors
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Endogenous CNP/GC-B signaling in fibroblasts merits targeted study; leaves open whether pathway agonism attenuates human cardiac fibrosis.
Endogenous C-type natriuretic peptide signaling via GC-B in cardiac fibroblasts exerts critical antifibrotic and antihypertrophic effects, particularly in females, suggesting a potential therapeutic target for pathological cardiac remodeling.
Werner et al. (2023) studied Cardiac fibrosis and adverse cardiac remodeling. Fibroblast-specific deletion of GC-B (Npr2) vs. Control littermates (Npr2fl/fl without Cre) was evaluated on Cardiac fibrosis and hypertrophy. Fibroblast-specific deletion of the CNP receptor GC-B in mice exacerbated cardiac fibrosis, hypertrophy, and contractile dysfunction in response to angiotensin II infusion or transverse aortic constriction, with more pronounced effects in females.
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