ArticleClinical and translational medicine2025
Irisin-mediated muscle-renal crosstalk as a protective mechanism against contrast-induced acute kidney injury via cGAS-STING signalling inhibition.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Complement activation and fibrinolysis dysregulation drive contrast-induced acute kidney injury: a 4D proteomics rat study.Renal failure · 2026Article
- Irisin upregulation as a contributory mechanism for the therapeutic benefits of SGLT-2 inhibitors.Pharmacology & therapeutics · 2026Review
- Irisin Restrains Oligodendroglial Ferroptosis to Preserve White Matter After Traumatic Brain Injury via AMPK Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Exercise-induced myokines in metabolic regulation: mechanisms, mimetics, and translational potential.Archives of pharmacal research · 2026Review
- IL-15 Links Muscle-Kidney Crosstalk to Preserving Podocyte Mitochondrial Fusion and Attenuating Diabetic Nephropathy.Journal of cachexia, sarcopenia and muscle · 2026Article
- Purpurin Rescues Contrast-Induced Acute Rat Kidney Injury via Inducing Autophagy and Inhibiting Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The dual role of the cGAS-STING signaling pathway in kidney diseases: from acute injury to chronic fibrosis - molecular mechanisms and precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- The mtDNA-cGAS-STING Axis in Acute Kidney Injury and Maladaptive Repair: Preclinical Evidence for Traditional Chinese Medicine and Natural Product-Based Interventions.Journal of inflammation research · 2026Review
- Glycyrrhizin alleviates contrast-induced acute kidney injury via inhibiting HMGB1-mediated renal tubular epithelial cells ferroptosis.Renal failure · 2025Article
- Irisin-mediated muscle-renal crosstalk as a protective mechanism against contrast-induced acute kidney injury via cGAS-STING signalling inhibition.Clinical and translational medicine · 2025Article
- Irisin Research Landscape (2012-2024): A Bibliometric and Visual Analysis of Evolving Hotspots and Future Trends.Biologics : targets & therapy · 2025Article
- Association of weight-adjusted waist index and Albuminuria in children and adolescents: A national population-based study.PloS one · 2025Article
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10 authors.
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Abstract
backgroundContrast-induced acute kidney injury (CI-AKI) continues to pose a pressing clinical challenge during invasive cardiovascular procedures due to the limited availability of preventative strategies. We aimed to demonstrate that irisin, a myokine induced by exercise, protects against CI-AKI by inhibiting the cGAS-STING inflammatory pathway. METHODS AND
resultsWe explored the relationship between serum irisin levels and CI-AKI incidence in patients administered the contrast media iohexol. Notably, lower serum irisin levels were strongly associated with an increased incidence of CI-AKI following contrast media administration. To establish a causal link between serum irisin levels and CI-AKI, we utilised a mouse model that simulates exercise by overexpressing muscle-specific PGC-1α. This approach showed a significant reduction in tubular injury and mitochondrial dysfunction induced by iohexol via cGAS/STING suppression, thereby diminishing inflammation. Mechanistically, irisin was found to inhibit the activation of cGAS/STING, preventing double stranded DNA (dsDNA) leakage and reducing inflammation in tubular epithelial cells (TECs). Pharmacological inhibition of STING further corroborated these observations. Moreover, we identified integrin complex αV/β5 as the irisin receptor on TECs, which is essential for irisin-mediated suppression of cGAS-STING signalling and resolution of inflammation.
conclusionsOur data position irisin as a crucial factor in muscle‒kidney crosstalk, inhibiting cGAS-STING signalling and preventing dsDNA leakage via integrin αV/β5 in TECs, thus mitigating tubular injury and inflammation. These data underscore the potential of irisin as both a predictive biomarker for CI-AKI and a promising candidate for preventative strategies against CI-AKI. HIGHLIGHTS: Irisin mediated muscle-kidney crosstalk mitigated tubular injury and inflammation. Irisin inhibited the cGAS-STING signalling activation via integrin αV/β5 in tubular epithelial cells. Irisin was a predictive biomarker and a promising candidate for CI-AKI.
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