Why the study?
Suberoylanilide hydroxamic acid has shown anti-fibrotic effects in various diseases, but whether it could suppress cardiac fibrosis remained to be evaluated.
Does suberoylanilide hydroxamic acid (SAHA) improve cardiac function and reduce fibrosis in mice with MI-induced cardiac fibrosis?
Does suberoylanilide hydroxamic acid (SAHA) improve cardiac function and reduce fibrosis in mice with MI-induced cardiac fibrosis?
SAHA demonstrates anti-fibrotic effects in MI-induced cardiac fibrosis through the TGF-β1/p38 pathway, suggesting potential as a therapeutic agent.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for HDAC inhibition in post-MI fibrosis; leaves open translation to human therapy.
Growing evidences have revealed that a histone deacetylase inhibitor (HDACi), suberoylanilide hydroxamic acid (SAHA) has anti-fibrotic effect in different diseases. In this study, we first evaluated whether SAHA could suppress cardiac fibrosis. Mice with MI-induced cardiac fibrosis were treated with SAHA by intraperitoneal injection and their cardiac function was improved after SAHA treatment. Results of western blotting and qRT-PCR in heart tissues suggested that TGFβ1/P38 pathway was activated in MI mice, and this effect was reversed by SAHA. Cell proliferation assay suggested that SAHA could suppress TGF-β1-induced cardiac fibroblasts proliferation. Furthermore, results of western blotting and qRT-PCR in cardiac fibroblasts depicted that SAHA may exert its anti-fibrotic effect through inhibiting TGF-β1-induced P38 phosphorylation by promoting DUSP4 expression. Our findings may substantiate SAHA as a promising treatment for MI-induced cardiac fibrosis.
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Wang et al. (2021) studied this question.
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