ArticleFrontiers in cell and developmental biology2026
Iron toxicity undermines microfracture-induced cartilage regeneration by predisposing a pre-ferroptotic niche.
Article in Frontiers in cell and developmental biology, 2026. 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
Microfracture (MF) often yields regenerated cartilage that resembles scar tissue and is prone to rapid deterioration. This outcome may be linked to elevated iron levels, which upregulate sphingolipid (SP) signaling and increase lipid exposure to reactive oxygen species (ROS), thereby heightening cellular sensitivity to iron. In this study, we analyze whether heme-derived iron released during clinical MF undermines cartilage regeneration. We compared regenerated and intact cartilage using histomorphological, proteomic, metabolomic, and transcriptional analyses. Regenerated tissue exhibited disrupted cellular organization and a deficient extracellular matrix. Omics profiling highlighted transferrin-mediated iron transfer, striking SP signaling, and increased oxidized glutathione tripeptide in cartilage regeneration. Integrated analysis further revealed a pre-ferroptotic microenvironment in newborn chondrocytes after MF, which is characterized by extracellular Fe
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