ArticlePharmaceutical biology2023
Metformin ameliorates ferroptosis in cardiac ischemia and reperfusion by reducing NOX4 expression via promoting AMPKα.
Article in Pharmaceutical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Eupatilin Alleviates Acute Myocardial Ischemia-Reperfusion Injury in Rats via the Akt/GSK-3β Pathway by Targeting COXs.Journal of biochemical and molecular toxicology · 2026Article
- Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway.Journal of cardiovascular translational research · 2026Article
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis: key regulatory pathways and their implications in cardiovascular pathophysiology.Frontiers in cardiovascular medicine · 2026Review
- Metformin alleviates lung ischemia‑reperfusion injury via the SIRT1 pathway following lung transplantation in diabetic rats.Molecular medicine reports · 2025Article
- Imeglimin Alleviates High-Glucose-Induced Bioenergetic and Oxidative Stress Thereby Enhancing Intercellular Adhesion in H9c2 Cardiomyoblasts.International journal of molecular sciences · 2025Article
- The Role of AMPKα in the Mechanism of Development and Treatment of Heart Failure.Reviews in cardiovascular medicine · 2025Review
- Electroacupuncture improves cardiac function in hyperlipidemic rats by enhancing efferocytosis in myocardial macrophages via the PPARγ-LXRα-MerTK pathway.Journal of traditional and complementary medicine · 2025Article
- Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Reviews in cardiovascular medicine · 2025Review
- Metformin-Sensitized Chemotherapy of Docetaxel Nanoemulsions Based on a Sequential Administration.Pharmaceutics · 2025Article
- Angiotensin type 1 and type 2 receptors-induced mitochondrial dysfunction promotes ferroptosis in cardiomyocytes.Journal of human hypertension · 2025Article
- Ferroptosis: mechanism and role in diabetes-related cardiovascular diseases.Cardiovascular diabetology · 2025Review
- Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.American journal of cardiovascular disease · 2025Review
- Unveiling the Protective Role of Metformin against Chemotherapy-induced Cardiotoxicity: A Comprehensive Scoping Review on Non-clinical Studies.Current medicinal chemistry · 2025Article
- Metformin improves intestinal ischemia-reperfusion injury by reducing the formation of mitochondrial associated endoplasmic reticulum membranes (MAMs) and inhibiting ferroptosis in intestinal cells.Frontiers in pharmacology · 2025Article
- Article
- From bench to bedside: targeting ferroptosis and mitochondrial damage in the treatment of diabetic cardiomyopathy.Frontiers in endocrinology · 2025Review
- Bone marrow mesenchymal stem cell-originated exosomes suppress activation of hepatic stellate cells through the miR-144-3p/SLC7A11 axis.Clinical and experimental hepatology · 2024Article
- HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis.Cell death & disease · 2024Article
- Effects of Trehalose Preconditioning on H9C2 Cell Viability and Autophagy Activation in a Model of Donation after Circulatory Death for Heart Transplantation.Current issues in molecular biology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextMetformin (Met) has a protective effect against cardiac ischemia and reperfusion (I/R) injury.
objectiveThis study uncovered the Met effect on ferroptosis in cardiac I/R. MATERIALS AND
methodsSprague-Dawley rats underwent cardiac I/R treatment (ischaemia 30 min; reperfusion 24 h) (I/R group), and administered intravenously with Met (200 mg/kg) (I/R + Met group). Haematoxylin-eosin staining, Prussian blue staining, immunohistochemistry and transmission electron microscope were conducted on cardiac tissues. H9c2 cells underwent oxygen-glucose deprivation/reoxygenation (OGD/R group) and treated by Met (0.1 mM) (OGD/R + Met group). Adenosine monophosphate-activated protein kinase α (AMPKα) siRNA was transfected into OGD/R-induced H9c2 cells. Cell counting kit-8 (CCK-8) assay, dichloro-dihydro-fluorescein diacetate (DCFH-DA) and JC-1 staining were conducted on H9c2 cells. Ferroptosis-related indicators and gene expression were detected by enzyme-linked immunosorbent assay (ELISA), quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot.
resultsIn cardiac I/R rat, Met decreased heart and serum MDA, cardiac and serum non-heme iron, and serum CK-MB and LDH (inhibition rate: 50.0%, 48.8%, 47.6%, 29.5%, 30.6% and 34.7%, respectively), relieved cardiac tissue ferroptosis and mitochondria damage, increased fraction shortening and ejection fraction (157.5% and 146.2% on day 28, respectively), up-regulated AMPKα and down-regulated NOX4 in cardiac tissues. In OGD/R-induced H9c2 cells, Met (0.1 mM) increased cell viability (promotion rate: 170.0%), decreased non-heme iron and MDA (inhibition rate: 30.1% and 47.9%, respectively), relieved ferroptosis, up-regulated AMPKα and down-regulated NOX4. AMPKα silencing abrogated these effects of Met on the OGD/R-induced H9c2 cells. DISCUSSION AND
conclusionsMet shows effectiveness in relieving ferroptosis in cardiac I/R. In the future, Met may be an effective drug for relieving ferroptosis in cardiac I/R patients clinically.
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