Crosstalk between ferroptosis and miRNA in type 2 diabetes mellitus and possible therapeutic targeting.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Type 2 diabetes (T2D) accounts for over 90% of diabetes mellitus and is characterized by peripheral tissue insulin resistance, a defective compensatory insulin secretion, and reduced insulin output from pancreatic β-cells. T2D is a complex metabolic syndrome involving multiple cell types within multiple organs, such as the liver, muscle, adipose tissue, and pancreas. Because the adult human endocrine pancreas does not have regenerative capability, understanding of the pathogenesis of T2D is vital for working out successful strategies for the delay or arrest of disease development. Newly, ferroptosis, an iron-dependent, regulated cell death, has emerged as a significant promoter of the pathogenesis and development of T2D. Ferroptosis is distinguishable from apoptosis, autophagy, and necroptosis, and is characterized by the accumulation of iron, lipid peroxidation, and suppression of glutathione peroxidase 4 (GPX4). Ferroptosis in pancreatic β-cells results in the defective secretion of insulin. The labile iron pool (LIP), particularly Fe 2 ⁺, enhances the formation of reactive oxygen species (ROS) during the Fenton reaction, thereby leading to ferroptosis. Recent empirical studies have revealed an exquisite regulatory interaction between ferroptosis and microRNAs (miRNAs), with the implication being that miRNAs play a central role in the regulation of ferroptosis during T2D. Two

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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