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Peer-reviewedCC BYAdvanced science (Weinheim, Baden-Wurttemberg, Germany)

Ischemic Postconditioning Protects Aged Myocardium Against Ischemia/Reperfusion Injury by Regulating Mitochondrial Dynamics via piR-4913.

  • Xiangyu Zhao1,2,3
  • Yanchun Li1,3
  • Nan Li1,3
  • Juan Zhang1,3
  • Xiaolong Ma1,3
  • Fei Yang1,3
  • Ruihan Long1,3
  • Yining Tian1,3
  • Yichen Wang1,3
  • Shengchao Ma1,3
  • Huiping Zhang4,5
  • Yideng Jiang1,3
5 affiliations
  1. 1NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, China.
  2. 2School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
  3. 3Ningxia Key Laboratory of Vascular Injury and Repair Research, Ningxia Medical University, Yinchuan, China.
  4. 4Department of Medical Genetics, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, China.
  5. 5Medical Experimental Center, General Hospital of Ningxia Medical University, Yinchuan, China.
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Abstract

Ischemic postconditioning (IPostC) mitigates myocardial ischemia/reperfusion (I/R) injury, but its regulation of mitochondrial dynamics in the aged heart remains unclear. This study investigates the underlying mechanisms by evaluating PIWI-interacting RNA (piRNA) expression profiles after I/R injury. Functional assays using piR-4913 silencing assess its impact on infarct size, mitochondrial ATP production, and oxidative stress. Mechanistic analyses identify that piR-4913, a cardiac-enriched piRNA markedly upregulated in aged hearts following I/R injury, is effectively suppressed by IPostC. Silencing piR-4913 confers cardioprotection by limiting infarct size, enhancing ATP production, and reducing oxidative stress. Mechanistically, piR-4913 acts as a key facilitator that promotes the recruitment of OGT to Drp1, thereby catalyzing the O-GlcNAcylation modification of Drp1 at Thr604. This modification promotes Drp1 mitochondrial translocation and Fis1 interaction, driving excessive mitochondrial fission and dysfunction. In vivo validation using a Drp1-T604A mutant demonstrates profound resistance to I/R injury, confirming the critical role of Thr604 O-GlcNAcylation in age-related cardiac damage. Collectively, IPostC exerts cardioprotection in the aging heart by restraining the piR-4913/OGT/Drp1 axis, thereby restoring mitochondrial proteostasis and dynamics. This pathway represents a promising therapeutic target to improve clinical outcomes in elderly patients with myocardial infarction.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026ischemic,
  title = {{Ischemic Postconditioning Protects Aged Myocardium Against Ischemia/Reperfusion Injury by Regulating Mitochondrial Dynamics via piR-4913.}},
  author = {Xiangyu Zhao and Yanchun Li and Nan Li and Juan Zhang and Xiaolong Ma and Fei Yang and Ruihan Long and Yining Tian and Yichen Wang and Shengchao Ma and Huiping Zhang and Yideng Jiang},
  journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
  year = {2026},
  month = oct,
  doi = {10.1002/advs.78464},
  url = {https://europepmc.org/article/MED/42949644},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Ischemic Postconditioning Protects Aged Myocardium Against Ischemia/Reperfusion Injury by Regulating Mitochondrial Dynamics via piR-4913.
AU  - Xiangyu Zhao
AU  - Yanchun Li
AU  - Nan Li
AU  - Juan Zhang
AU  - Xiaolong Ma
AU  - Fei Yang
AU  - Ruihan Long
AU  - Yining Tian
AU  - Yichen Wang
AU  - Shengchao Ma
AU  - Huiping Zhang
AU  - Yideng Jiang
PY  - 2026
DA  - 2026/10/28
JO  - Advanced science (Weinheim, Baden-Wurttemberg, Germany)
DO  - 10.1002/advs.78464
UR  - https://europepmc.org/article/MED/42949644
AB  - Ischemic postconditioning (IPostC) mitigates myocardial ischemia/reperfusion (I/R) injury, but its regulation of mitochondrial dynamics in the aged heart remains unclear. This study investigates the underlying mechanisms by evaluating PIWI-interacting RNA (piRNA) expression profiles after I/R injury. Functional assays using piR-4913 silencing assess its impact on infarct size, mitochondrial ATP production, and oxidative stress. Mechanistic analyses identify that piR-4913, a cardiac-enriched piRNA markedly upregulated in aged hearts following I/R injury, is effectively suppressed by IPostC. Silencing piR-4913 confers cardioprotection by limiting infarct size, enhancing ATP production, and reducing oxidative stress. Mechanistically, piR-4913 acts as a key facilitator that promotes the recruitment of OGT to Drp1, thereby catalyzing the O-GlcNAcylation modification of Drp1 at Thr604. This modification promotes Drp1 mitochondrial translocation and Fis1 interaction, driving excessive mitochondrial fission and dysfunction. In vivo validation using a Drp1-T604A mutant demonstrates profound resistance to I/R injury, confirming the critical role of Thr604 O-GlcNAcylation in age-related cardiac damage. Collectively, IPostC exerts cardioprotection in the aging heart by restraining the piR-4913/OGT/Drp1 axis, thereby restoring mitochondrial proteostasis and dynamics. This pathway represents a promising therapeutic target to improve clinical outcomes in elderly patients with myocardial infarction.
SN  - 2198-3844
ER  -