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Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5

Xiang-Bo An1, Yi-Tong Wang2, Xin Liu3

  • 1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chao Yang District, Beijing, 100029, China. anxiangbo@pku.org.cn.

Journal of Cardiovascular Translational Research
|May 19, 2026
PubMed

Insights

Xanthatin effectively treats pathological cardiac hypertrophy by suppressing CREB5 signaling. This study reveals the Xanthatin-CREB5 axis as a promising therapeutic target for heart failure.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Pathological cardiac hypertrophy is a significant risk factor for heart failure.
  • The therapeutic potential of Xanthatin in cardiac hypertrophy was previously unexplored.

Purpose of the Study:

  • To investigate the effects of Xanthatin on pathological cardiac hypertrophy.
  • To identify the molecular target through which Xanthatin exerts its effects.

Main Methods:

  • A mouse model of Angiotensin II (Ang II)-induced cardiac hypertrophy was utilized.
  • Echocardiography and histology were employed to assess cardiac function and structure.
  • Adeno-associated virus serotype 9 (AAV9) vectors were used for cardiac-specific overexpression or knockdown of CREB5.

Main Results:

  • Xanthatin treatment significantly reduced Ang II-induced cardiac hypertrophy, oxidative stress, fibrosis, and inflammation.
  • Overexpression of CREB5 diminished Xanthatin's protective effects, while CREB5 knockdown enhanced them.
  • Xanthatin's beneficial actions are dependent on the modulation of CREB5 signaling.

Conclusions:

  • Xanthatin is a potent inhibitor of Ang II-induced pathological cardiac hypertrophy.
  • The protective mechanism of Xanthatin involves the suppression of CREB5 signaling.
  • The Xanthatin-CREB5 axis represents a novel therapeutic target for pathological cardiac remodeling and heart failure.

Keywords:
Angiotensin IICREB5Cardiac hypertrophyXanthatin

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