ArticleAnatolian journal of cardiology2019
Treatment with metformin prevents myocardial ischemia-reperfusion injury via STEAP4 signaling pathway.
Article in Anatolian journal of cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- From Diabetes to Degenerative Diseases: The Multifaceted Action of Metformin.International journal of molecular sciences · 2025Review
- Metformin ameliorates ferroptosis in cardiac ischemia and reperfusion by reducing NOX4 expression via promoting AMPKα.Pharmaceutical biology · 2023Article
- Effects of Metformin on Ischemia/Reperfusion Injury: New Evidence and Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Stamp2 Protects From Maladaptive Structural Remodeling and Systolic Dysfunction in Post-Ischemic Hearts by Attenuating Neutrophil Activation.Frontiers in immunology · 2021Article
- Metformin Alleviates Left Ventricular Diastolic Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aims to investigate the underlying mechanism of metformin in reducing myocardial apoptosis and improving mitochondrial function in rats and H9c2 cells subjected with myocardial ischemia-reperfusion injury (I/R).
methodFollowing pretreatment with metformin, male Sprague-Dawley (SD) rats were used to establish an ischemia-reperfusion (I/R) model in vivo. Serum creatinine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were examined by ELISA. Infarct size and apoptosis were measured by TTC staining and TUNEL assay. Pathological changes were evaluated by HE staining. H9c2 cells were used to establish a hypoxia-reoxygenation (H/R) model in vitro. Cell apoptosis and mitochondrial membrane potential (MMP) were examined by flow cytometry and Rhodamine 123. The expression levels of STEAP4, Bcl-2, Bax and GAPDH in both myocardial tissues and H9c2 cells were determined by western blotting.
resultsWe found that metformin decreased infarct size, increased expression of STEAP4, mitigated myocardial apoptosis and increased mitochondrial membrane potential (MMP) when the models were subjected to H/R or I/R injuries. However, STEAP4 knockdown significantly abrogated the beneficial effect of metformin.
conclusionsWe further demonstrated the protective effect of metformin on cardiomyocytes, which might be at least partly attributable to upregulation of STEAP4. Therefore, STEAP4 might be a new target to decrease apoptosis and rescue mitochondrial function in myocardial ischemia-reperfusion injury.
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