ArticleRenal failure2025
Irisin targets the HK1-glycolysis-NLRP3 pyroptosis axis to prevent chronic kidney disease-associated vascular calcification.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Vascular calcification (VC) in chronic kidney disease (CKD) remains a critical clinical challenge with limited therapeutic options. This study investigates the regulatory role of HK1-mediated glycolysis in NLRP3 inflammasome-driven pyroptosis during chronic kidney disease (CKD)-associated vascular calcification (VC) and the protective effects of Irisin/FNDC5. Using β-glycerophosphate-treated vascular smooth muscle cells (VSMCs) and CKD mouse models, we employed transcriptomic analysis, FNDC5 genetic knockout, and overexpression strategies to dissect HK1's mechanistic contribution. Results revealed that HK1-dependent glycolysis amplifies NLRP3 inflammasome activation and pyroptosis in calcifying VSMCs, while Irisin suppressed HK1 expression and glycolytic flux, thereby inhibiting NLRP3-driven pyroptosis. Irisin precursor Fndc5 knockout exacerbated aortic calcification and upregulated HK1-NLRP3 signaling in CKD mice, whereas Irisin administration reversed these effects. This study demonstrates that HK1-driven glycolysis acts as a metabolic driver of NLRP3-mediated pyroptosis in CKD-associated vascular calcification. Irisin suppresses this HK1-glycolysis-inflammasome axis, thereby attenuating vascular smooth muscle cell pyroptosis and calcification. These findings reveal a previously unrecognized HK1-glycolysis-NLRP3 pathway as a metabolic-inflammatory target and suggest that Irisin/HK1 modulation may represent a novel therapeutic strategy for CKD-related vascular calcification.
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