ArticleDiabetology & metabolic syndrome2025
Irisin regulates integrin αvβ5/FAK/ERK to inhibit neutrophil extracellular traps formation and reduce pancreatic beta-cells pyroptosis in type 2 diabetes mellitus.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The myokine irisin ameliorates the secretory dysfunction of pancreatic β cells in experimental and human type 2 diabetes.Science advances · 2026Article
- Neutrophils and neutrophil extracellular traps in diabetes mellitus and its complications: Mechanisms and therapeutic implications.iScience · 2026Review
- Exercise-Induced Irisin: A Novel Strategy for Neuroinflammation Alleviation and Neurorepair in Diabetic Retinopathy.International journal of molecular sciences · 2026Review
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6 authors.
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Abstract
backgroundDysregulation of neutrophil extracellular traps (NETs), through overproduction or poor clearance, can lead to tissue damage and is linked to inflammatory conditions like type 2 diabetes mellitus (T2DM). Irisin, a hormone believed to modulate energy metabolism and enhance insulin sensitivity, holds promise as a potential treatment for T2DM. This study aims to investigate the role of Irisin in alleviating β-cell pyroptosis by inhibiting NETs formation and elucidating the underlying molecular mechanisms.
methodsC57BL/6J mice were used to establish T2DM through a high-fat diet and streptozotocin injection. Glucose metabolism was evaluated using oral glucose tolerance tests and fasting plasma insulin measurements. Histological analysis of pancreatic tissue was carried out using hematoxylin and eosin staining, while the formation of NETs was assessed through immunofluorescent staining. In vitro, Min6 cells were cultured under high-glucose conditions to simulate T2DM, and treated with Irisin. Irisin's impact on NETs was determined using Sytox Green staining. Key signaling molecules were examined with Western blotting.
resultsIrisin treatment improved glucose tolerance, increased insulin levels, and reduced NETs formation in T2DM mice. Histological analysis showed decreased pancreatic tissue damage. In vitro, Irisin inhibited NETs formation through the αVβ5/FAK/ERK pathway and reduced NETs-induced pyroptosis in β-cells via the STING/IRE1α/NLRP1 pathway. Blocking these pathways confirmed Irisin's protective role against NETs-mediated pyroptosis.
conclusionIrisin exhibits protective effects against β-cell pyroptosis in T2DM by inhibiting NETs formation through integrin-related signaling pathways. These findings suggest that Irisin may serve as a therapeutic agent in managing T2DM by modulating NETs and preserving β-cell function.
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