Key result
PCSK9 upregulated profibrotic activities in cardiac fibroblasts, while PCSK9 inhibition with alirocumab improved left ventricular systolic function and attenuated fibrosis in heart failure rats.
Why the study?
PCSK9 correlates with mortality in heart failure, but whether PCSK9 increases cardiac fibroblast activities and its underlying mechanisms remained unclear.
Population
Human cardiac fibroblasts and isoproterenol-induced HF rats
Comparison
PCSK9 exposure in vitro and alirocumab treatment in HF rats vs controls
Design
Preclinical in vitro and in vivo laboratory study
Follow-up
28 consecutive days
Authors
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May warrant caution in HF fibrosis management; leaves open whether PCSK9 inhibition confers clinical benefit.
PCSK9 promotes cardiac fibrosis via TLR4 and NLRP3 inflammasome signaling, and its inhibition with alirocumab improves cardiac function and reduces fibrosis in a rat model of heart failure.
Chung et al. (2025) studied Heart failure and cardiac fibrosis. PCSK9 (in vitro) and Alirocumab (in vivo) vs. Control cells / untreated heart failure rats was evaluated on Fibroblast proliferation, myofibroblast differentiation, collagen production, left ventricular systolic function, and fibrosis. PCSK9 upregulated profibrotic activities in cardiac fibroblasts, while PCSK9 inhibition with alirocumab improved left ventricular systolic function and attenuated fibrosis in heart failure rats.
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