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<p>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.</p> Graphical Abstract <p></p>

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Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5

  • 期刊论文

  • 发表日期：

    2026年5月19日

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  • Xiang-Bo An,
  • Yi-Tong Wang,
  • Xin Liu,
  • Fei Gao,
  • Zhi-Jian Wang

摘要

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.

Graphical Abstract