ArticleThe Kaohsiung journal of medical sciences2020
MiR-129-5p alleviates myocardial injury by targeting suppressor of cytokine signaling 2 after ischemia/reperfusion.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- miRNA-Mediated Regulation of γ-Globin to β-Globin Switching: Therapeutic Potential in β-Hemoglobinopathies.International journal of molecular sciences · 2026Review
- Extracellular vesicles in osteoarthritis: mechanisms, therapeutic potential, and diagnostic applications.Frontiers in immunology · 2025Review
- Cardiovascular Disease and miRNAs: Possible Oxidative Stress-Regulating Roles of miRNAs.Antioxidants (Basel, Switzerland) · 2024Review
- Endocardial HDAC3 is required for myocardial trabeculation.Nature communications · 2024Article
- Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p.Iranian journal of public health · 2022Article
- Mesenchymal Stem Cell-Derived Exosome-Loaded microRNA-129-5p Inhibits TRAF3 Expression to Alleviate Apoptosis and Oxidative Stress in Heart Failure.Cardiovascular toxicology · 2022Article
- Mycobacterium avium subsp. paratuberculosis exploits miRNA expression to modulate lipid metabolism and macrophage polarisation pathways during infection.Scientific reports · 2022Article
- Regulatory role of miR-129 and miR-384-5p on apoptosis induced by oxygen and glucose deprivation in PC12 cell.Experimental brain research · 2022Article
- MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway.International journal of molecular medicine · 2021Article
- miR-129 Attenuates Myocardial Ischemia Reperfusion Injury by Regulating the Expression of PTEN in Rats.BioMed research international · 2021Article
- MiR-129-5p alleviates myocardial injury by targeting suppressor of cytokine signaling 2 after ischemia/reperfusion.The Kaohsiung journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction (AMI) remains one of the leading causes of morbidity and mortality worldwide. Ischemia/reperfusion (I/R), the most common consequence of AMI treatment, may induce severe myocardial cell injury, yet the precise mechanism continues to be enigmatic. In the present study, we found that miR-129-5p was significantly downregulated in mouse I/R model. Then, we overexpressed miR-129-5p via intravenous injection of specific miR-129-5p agomir before I/R model establishment. MiR-129-5p overexpression dramatically alleviated myocardial injury in I/R mice as evidenced by reduced lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) content, and infract size. We further detected the effect of miR-129-5p on hypoxia/reoxygenation (H/R)-induced H9C2 cell in vitro. MiR-129-5p overexpression improved H9C2 cell viability and inhibited cell apoptosis induced by H/R, accompanied with decreased LDH activity and MDA content. Besides, luciferase reporter assay indicated that suppressor of cytokine signaling 2 (SOCS2) was a downstream target of miR-129-5p. SOCS2 was upregulated in H/R induced H9C2 cells, and miR-129-5p overexpression suppressed SOCS2 expression at both mRNA and protein levels. In addition, SOCS2 overexpression abolished the protective effects of miR-129-5p on H/R-induced H9C2 cells, concomitant with elevated expression of apoptosis-related cleaved poly-(ADP-ribose) polymerase and cleaved caspase-3. In conclusion, our results demonstrated that miR-129-5p alleviated myocardial injury induced by I/R both in vitro and in vivo, and miR-129-5p/SOCS2 axis is a potential therapeutic target for alleviating myocardial injury in AMI patients after reperfusion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.