2. Academic Validation
  3. Yixinshu attenuates myocardial infarction via SHP1/JAK2/STAT3-mediated regulation of mitochondrial function and apoptosis

Yixinshu attenuates myocardial infarction via SHP1/JAK2/STAT3-mediated regulation of mitochondrial function and apoptosis

  • Chin Med. 2026 Mar 4;21(1):76. doi: 10.1186/s13020-025-01299-4.
Xueting Wang # 1 2 3,  Xinrui Wang # 1 2 3,  Yang Liu 1 2 3,  Yang Cui 1 2 3,  Keyi Chen 1 2 3,  Hongkun Wu 4,  Mingshan Zhang 1 2 3,  Ming Liao 5,  Linyun Fu 6 7 8,  Xiangchun Shen 9 10 11
Affiliations

Affiliations

  • 1 The State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
  • 2 The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province and The High Educational Key Laboratory of Guizhou Province for Natural Medicinal Pharmacology and Druggability (Guizhou International Science and Technology Cooperation Base for Druggability Research of Natural Medicines), Guizhou Medical University, Guiyang, Guizhou, China.
  • 3 The Key Laboratory of Optimal Utilization of Natural Medicine Resources (The Union Key Laboratory of Guiyang City-Guizhou Medical University), School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, Guizhou, China.
  • 4 Department of Cardiac Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.
  • 5 The Maternal and Child Health Hospital of Guiyang City, Guiyang, Guizhou, China. [email protected].
  • 6 The State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • 7 The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province and The High Educational Key Laboratory of Guizhou Province for Natural Medicinal Pharmacology and Druggability (Guizhou International Science and Technology Cooperation Base for Druggability Research of Natural Medicines), Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • 8 The Key Laboratory of Optimal Utilization of Natural Medicine Resources (The Union Key Laboratory of Guiyang City-Guizhou Medical University), School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • 9 The State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • 10 The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province and The High Educational Key Laboratory of Guizhou Province for Natural Medicinal Pharmacology and Druggability (Guizhou International Science and Technology Cooperation Base for Druggability Research of Natural Medicines), Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • 11 The Key Laboratory of Optimal Utilization of Natural Medicine Resources (The Union Key Laboratory of Guiyang City-Guizhou Medical University), School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, Guizhou, China. [email protected].
  • # Contributed equally.
PMID: 41782161 DOI: 10.1186/s13020-025-01299-4
Abstract

Yixinshu (YXS), a traditional Chinese formula, is applied for coronary artery diseases in clinic, however, its cardioprotective mechanisms remain unclear. At present, the role and underlying mechanisms of YXS is to elucidate in enhancing post-myocardial infarction (MI) recovery. MI mouse models and hypoxia-injured cardiomyocytes were reproduced to evaluate YXS efficacy. The pharmacological targets and blood-absorbed compounds of YXS were determined by network pharmacology and LC-MS, respectively. Bioactive components were screened via molecular docking and surface plasmon resonance (SPR), and mechanisms were validated by molecular assays. YXS improved cardiac function and reduced infarct size. These effects were linked to preserved mitochondrial homeostasis and reduced Apoptosis through the SHP1/JAK2/STAT3 pathway. Dihydrotanshinone Ⅰ (DHT), a key compound identified in plasma, suppressed SHP1, activated STAT3, and mitigated mitochondrial injury. SHP1 overexpression could abolish DHT's protection effects. Taken together, YXS could exert cardioprotection in MI by modulating mitochondrial function and Apoptosis via the SHP1/JAK2/STAT3 axis, and DHT is potential beneficial bioactive ingredient mediating these effects.

Keywords

Apoptosis; Dihydrotanshinone I; Myocardial infarction; SHP1; Yixinshu.

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