Metformin again? Atheroprotection mediated by macrophage AMPK and ATF1
Abstract
This editorial refers to ‘Metformin directly suppresses atherosclerosis in normoglycemic mice via haematopoietic Adenosine Monophosphate-Activated Protein Kinase (AMPK)’ by A. Seneviratne et al., pp.1295–1308. Metformin is a biguanide that has been used as a frontline treatment for type 2 diabetes (T2DM) over the past 60 years, though its medicinal roots date back to medieval times. While new medications have emerged in recent years, metformin remains the most widely prescribed anti-diabetic drug. Despite this, the molecular mechanisms by which metformin acts remain incompletely understood.1 Twenty years ago, metformin was demonstrated to activate hepatic AMP-activated protein kinase (AMPK),2 a master regulator of energy homeostasis that exerts control over lipid and carbohydrate metabolism. Although metformin-mediated suppression of hepatic glucose production was subsequently shown to be AMPK-independent,3 others reported that AMPK activation underlies metformin-mediated improvements in insulin action by maintaining hepatic lipid homeostasis.4 Given its low cost, well-known tolerance and broad metabolic benefits, there are efforts currently underway to ‘repurpose’ metformin towards conditions, such as cancers, ageing, and cardiovascular disease. Atherosclerosis is characterized by chronic-low-grade inflammation that is driven by hyperlipidaemia and immune-infiltration that results in the formation of lipid-rich plaque in the arterial intima. Atherosclerotic macrovascular…
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