ArticleJournal of cardiovascular translational research2026
Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5.
Article in Journal of cardiovascular translational research, 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
Pathological cardiac hypertrophy is a key precursor to heart failure. The role of Xanthatin in this process was unknown. This study aimed to investigate its effects and molecular target. A mouse model of Ang II-induced hypertrophy was used. Xanthatin's effects were assessed by echocardiography and histology. Cardiac-specific overexpression or knockdown of CREB5 was performed using AAV9-cTNT vectors during Ang II and Xanthatin co-treatment to validate its functional role. Xanthatin treatment significantly alleviated Ang II-induced cardiac hypertrophy, oxidative stress, fibrosis, and inflammation. Crucially, cardiac-specific overexpression of CREB5 markedly attenuated these protective effects of Xanthatin. Conversely, cardiac-specific knockdown of CREB5 synergized with Xanthatin, further enhancing its suppressive actions on all pathological hallmarks. Xanthatin is a potent inhibitor of Ang II-induced cardiac hypertrophy, and its protective effect is mediated through the suppression of CREB5 signaling. This identifies the Xanthatin-CREB5 axis as a novel and promising therapeutic target for pathological cardiac remodeling.
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