Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1

Post time 2026-10-17 18:58:29

Journal：Cardiovascular Drugs and Therapy
Authors：Lang She, Hua Tu, Yin-Zhuang Zhang, Li-Jing Tang, Nian-Sheng Li, Qi-Lin Ma, Bin Liu, Qingjie Li, Xiu-Ju Luo, Jun Peng
Published date：2019
DOI：10.1007/s10557-018-06848-8
PMID：30637549
PDF link：https://link.springer.com/content/pdf/10.1007/s10557-018-06848-8.pdf
Article link：https://doi.org/10.1007/s10557-018-06848-8
PubMed link：https://pubmed.ncbi.nlm.nih.gov/30637549/
Article Source：Springer Nature / PubMed
Article Title：Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1
Content：
This study investigates the role of phosphoglycerate mutase 5 (PGAM5) in myocardial ischemia/reperfusion injury and examines whether its inhibition can reduce necroptosis, a regulated form of cell death.
The researchers used a rat heart ischemia/reperfusion model and an H9c2 cardiac cell model to investigate the relationship between PGAM5, dynamin-related protein 1 (Drp1), mitochondrial dysfunction, and necroptosis-associated signalling.
The findings indicated that PGAM5 inhibition reduced indicators of myocardial injury and necroptosis and suppressed Drp1-associated mechanisms. The study also investigated the relationship between PGAM5 and RIPK1-related signalling.
Conclusion：
The study suggests that PGAM5 may be a potential molecular target for reducing myocardial ischemia/reperfusion injury. Its findings provide a basis for further research into cardioprotective therapeutic strategies for acute myocardial infarction.
Relevance to AI-Driven Drug Discovery for Acute Myocardial Infarction：
This paper can support literature review, molecular-target identification, mechanism analysis, and candidate-compound prioritisation. PGAM5 and Drp1 may be investigated as potential targets for reducing mitochondrial dysfunction and cardiac cell death.
Limitations：
The research is preclinical and does not establish safety or efficacy in humans. Further validation, pharmacological studies, and safety assessments are necessary before considering clinical applications.
Remark：
Relevant preclinical mechanistic research on myocardial ischemia/reperfusion injury. The findings should be treated as preliminary evidence for target discovery, not as proof of an effective emergency treatment for heart attack patients.

Post time 2026-10-17 18:58:30

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