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<p>Metformin, a biguanide produced from <i>Galega officinalis</i>, is the most commonly used first-line treatment for type 2 diabetes mellitus (T2DM). Beyond its traditional glucose-lowering actions, which involve inhibiting hepatic gluconeogenesis and increasing insulin sensitivity, accumulating data suggest that it has multifaceted benefits for cardiovascular health. Metformin acts by activating AMP-activated protein kinase (AMPK), lowering oxidative stress and inflammation while enhancing lipid metabolism, energy homeostasis, and endothelial nitric oxide (eNOS) generation. It has been effective in reducing cardiac ischemia–reperfusion (I/R) injury, improving endothelial dysfunction, and modifying the autophagy and apoptosis pathways in cardiomyocytes. New research suggests that metformin’s modulation of gut microbiota, particularly the enrichment of <i>Akkermansia muciniphila</i> and short-chain fatty acid (SCFA) -producing bacteria, contributes to its cardiometabolic benefits by improving intestinal barrier integrity and lowering circulating Trimethylamine N-oxide (TMAO) levels. Clinical trials, such as United Kingdom Prospective Diabetes Study (UKPDS) and Metformin for Left Ventricular Hypertrophy Regression in Coronary Artery Disease (MET-REMODEL), as well as current studies like Metformin in Heart Failure Trial (MET-HEFT) and Veterans Affairs–Investigation of Metformin in Prediabetes on Atherosclerotic Cardiovascular Outcomes Trial (VA-IMPACT), are investigating metformin’s cardiovascular effects in addition to its glycemic management. Despite increasing evidence of metformin’s cardioprotective benefits, the combination of molecular, clinical, and gut microbiota-mediated processes has received little attention. This review seeks to offer a complete assessment of the existing data relating metformin’s cardioprotective activities to developing microbiota-related pathways and clinical outcomes.</p> Graphical Abstract <p></p>

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Cardioprotective Actions of Metformin in Myocardial Infarction: Molecular Mechanisms and Clinical Perspectives

  • 期刊论文

  • 发表日期：

    2026年7月10日

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  • Krushna Ch Maharana,
  • Sanjiv Singh,
  • Md. Abubakar,
  • Shricharan Pandey

摘要

Metformin, a biguanide produced from Galega officinalis, is the most commonly used first-line treatment for type 2 diabetes mellitus (T2DM). Beyond its traditional glucose-lowering actions, which involve inhibiting hepatic gluconeogenesis and increasing insulin sensitivity, accumulating data suggest that it has multifaceted benefits for cardiovascular health. Metformin acts by activating AMP-activated protein kinase (AMPK), lowering oxidative stress and inflammation while enhancing lipid metabolism, energy homeostasis, and endothelial nitric oxide (eNOS) generation. It has been effective in reducing cardiac ischemia–reperfusion (I/R) injury, improving endothelial dysfunction, and modifying the autophagy and apoptosis pathways in cardiomyocytes. New research suggests that metformin’s modulation of gut microbiota, particularly the enrichment of Akkermansia muciniphila and short-chain fatty acid (SCFA) -producing bacteria, contributes to its cardiometabolic benefits by improving intestinal barrier integrity and lowering circulating Trimethylamine N-oxide (TMAO) levels. Clinical trials, such as United Kingdom Prospective Diabetes Study (UKPDS) and Metformin for Left Ventricular Hypertrophy Regression in Coronary Artery Disease (MET-REMODEL), as well as current studies like Metformin in Heart Failure Trial (MET-HEFT) and Veterans Affairs–Investigation of Metformin in Prediabetes on Atherosclerotic Cardiovascular Outcomes Trial (VA-IMPACT), are investigating metformin’s cardiovascular effects in addition to its glycemic management. Despite increasing evidence of metformin’s cardioprotective benefits, the combination of molecular, clinical, and gut microbiota-mediated processes has received little attention. This review seeks to offer a complete assessment of the existing data relating metformin’s cardioprotective activities to developing microbiota-related pathways and clinical outcomes.

Graphical Abstract