Authors
Faiz Qamar, Tufail Ahmad, Divya Vohora, Manju Sharma
Published in
Molecular biology reports. Volume 53. Issue 1. Jun 23, 2026. Epub Jun 23, 2026.
Abstract
Diabetes mellitus (DM) is increasingly recognized as a major risk factor for skeletal fragility, characterized by impaired bone quality and increased fracture susceptibility. Chronic hyperglycemia induces metabolic stress, oxidative injury, and low-grade inflammation, all of which disrupt normal bone remodeling. Accumulating evidence indicates that pyroptosis, a highly inflammatory form of programmed cell death, has emerged as a critical mechanistic link between diabetes and bone loss. Pyroptosis is driven by inflammasome activation, particularly the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, leading to caspase-1 activation, gasdermin-mediated membrane pore formation, and the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). In the diabetic bone microenvironment, pyroptosis affects all major bone cell types. Osteoblast pyroptosis suppresses bone formation, osteoclast-associated pyroptotic signaling enhances bone resorption, and osteocyte pyroptosis disrupts mechanotransduction and microarchitectural integrity. Emerging data further reveal extensive crosstalk between pyroptosis, apoptosis, and necroptosis through PANoptotic signaling pathways, amplifying inflammatory bone damage. Experimental evidence from in vivo and in vitro models, together with emerging biomarker studies, consistently supports a central role for pyroptosis in diabetes-associated bone disease. Understanding the molecular regulation and temporal dynamics of pyroptosis in bone may provide novel therapeutic opportunities to preserve skeletal health in diabetic patients.
PMID:
42334693
Bibliographic data and abstract were imported from PubMed on 23 Jun 2026.
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