ArticleBMC cardiovascular disorders2026
Captopril alleviates doxorubicin-induced cardiac fibrosis and pyroptosis through mechanisms related to the PKN1-Rho/ROCK pathways.
Article in BMC cardiovascular disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDoxorubicin (DOX)-induced cardiac fibrosis and pyroptosis are critical processes contributing to heart failure. This in vitro study examines the protective role of captopril (CTL) in H9c2 cardiomyoblasts, emphasizing the potential involvement of the PKN1-associated Rho/ROCK signaling pathway.
methodsH9c2 cells were exposed to DOX to induce fibrosis and pyroptosis, followed by CTL treatment. Molecular docking was used to predict CTL-PKN1 interactions. Gene and protein expression were analyzed by RT-qPCR, Western blot, and immunofluorescence. Cell proliferation was assessed using CCK-8, EdU, and flow cytometry assays, while pyroptosis markers were quantified by Western blot.
resultsCTL significantly attenuated DOX-induced fibrosis by downregulating Collagen I, Collagen III, and α-SMA expression. Molecular docking analysis indicated astrong CTL-PKN1 interaction. CTL also suppressed Rho/ROCK pathway activation, whereas PKN1 overexpression reversed CTL's protective effects, confirming PKN1's key regulatory role. Additionally, CTL reduced pyroptosis-related proteins, including GSDMD and caspase-1, and decreased cell death.
conclusionCTL protects H9c2 cells from DOX-induced cardiac fibrosis and pyroptosis, possibly through modulation of the PKN1-associated Rho/ROCK signaling pathway, highlighting its potential as a therapeutic candidate for cardiac fibrosis-related diseases.
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