Key result
Apelin prevents structural remodeling and ventricular dysfunction in mice via a SphK1-dependent mechanism.
Why the study?
Whether apelin is involved in cardiac fibroblast activation, myofibroblast formation, and cardiac fibrotic remodelling remains unknown.
Does apelin prevent cardiac fibroblast activation and fibrotic remodeling in mouse models of pressure overload?
Does apelin prevent cardiac fibroblast activation and fibrotic remodeling in mouse models of pressure overload?
Apelin prevents cardiac fibroblast activation and structural remodeling through a SphK1-dependent mechanism, suggesting a potential therapeutic target for progressive heart failure.
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Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“administration of apelin has been demonstrated to blunt cardiac fibroblast activation and fibrosis”
Apelin pathways merit exploration as anti-fibrotic targets in heart failure; leaves open whether this extends to clinical outcomes.
Pchejetski et al. (2011) studied Cardiac fibrosis. Apelin was evaluated on Cardiac fibroblast activation, collagen production, and myocardial fibrotic remodelling. Apelin inhibited TGF-β-stimulated activation of cardiac fibroblasts and prevented structural remodelling and ventricular dysfunction in a mouse aortic banding model via a SphK1-dependent mechanism.
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