ArticleScientific reports2025
Quantitative LFQ-DIA proteomics reveals FTH1-MCM5/WNT axis mediated osteoblastic dysfunction via ferroptosis drives diabetic osteoporosis.
Article in Scientific reports, 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
In diabetes mellitus osteoporosis (DMOP), a common and severe chronic complication of diabetes mellitus (DM), long-term challenges are posed to public health. Recent evidence has implicated ferroptosis-a form of regulated cell death driven by iron-dependent lipid peroxidation-in the pathogenesis of DMOP. Ferritin heavy chain 1 (FTH1) plays a critical role in regulating iron metabolism during ferroptosis. To elucidate the regulatory mechanisms by which FTH1 modulates osteoblast (OB) ferroptosis and aberrant bone metabolism under high glucose and high fat (HGHF) conditions, we performed quantitative LFQ-DIA proteomics combined with bioinformatic analysis. MC3T3-E1 cells cultured under high glucose and high palmitic acid (HGPA) conditions were subjected to lentiviral-mediated FTH1 knock down (KD) or over expression (OE), and their protein expression profiles were systematically compared. We identified 857 differentially expressed proteins (DEPs) in the FTH1
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