Volume 29 Issue 10
Oct.  2025
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Article Navigation >  Chinese Journal of General Practice  > 2025  >  23(10): 1654-1657
ZHOU Ruiling, SUN Jinghui, DENG Yanping, HUANG Hongbo, NIU Zelong, WANG Peili. Exploring potential molecular targeting strategies for the treatment of acute myocardial infarction with genes encoding panax notoginseng saponins[J]. Chinese Journal of General Practice, 2025, 23(10): 1654-1657. doi: 10.16766/j.cnki.issn.1674-4152.004198
Citation: ZHOU Ruiling, SUN Jinghui, DENG Yanping, HUANG Hongbo, NIU Zelong, WANG Peili. Exploring potential molecular targeting strategies for the treatment of acute myocardial infarction with genes encoding panax notoginseng saponins[J]. Chinese Journal of General Practice, 2025, 23(10): 1654-1657. doi: 10.16766/j.cnki.issn.1674-4152.004198
shu

Exploring potential molecular targeting strategies for the treatment of acute myocardial infarction with genes encoding panax notoginseng saponins

doi: 10.16766/j.cnki.issn.1674-4152.004198
  • 1.

    National Research Center of Chinese Medicine and Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China

Funds:

 82305028

  • Received Date: 2025-01-10
    Abstract
  •   Objective  To analyze the causal relationship between genes underlying the antithrombotic drug target of Panax notoginseng saponins (PNS) and acute myocardial infarction (AMI) using Mendelian randomization (MR) method.  Methods  Genome-wide association study (GWAS) datasets were obtained from the European Bioinformatics Institute, Finnish database and UK Biobank database, all available online at the IEU Open GWAS website. Random-effects inverse variance weighting was the main analytical method, MR-Egger regression tested for horizontal pleiotropy, Cochran' s Q test assessed heterogeneity, and leave-one-out sensitivity analysis assessed stability.  Results  Eighteen core drug targets of PNS were obtained, and the genetic proxies of the 18 targets were screened for thrombus-positive diseases to identify 11 effective antithrombotic targets, which resulted in five potential drug targets for the treatment of AMI, including HIF1A, MDM2, CCND1, TP53 and INS. PNS targets HIF1A, CCND1, TP53, and INS were associated with an increased risk of AMI (all OR>1, P<0.05), and MDM2 was associated with a decreased risk of AMI (OR=0.671, P=0.022).  Conclusion  PNS exhibits potential therapeutic effects for AMI by targeting myocardial apoptosis pathways through antithrombotic genes to modulate disease progression, highlighting its potential as a key target for developing precision therapeutic strategies.

     

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