ReviewThe Journal of clinical investigation2026
Ferroptosis as a target mechanism in heart and kidney disease.
Review in The Journal of clinical investigation, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
Funding
Abstract
Ferroptosis is a distinct form of regulated cell death driven by lipid peroxidation and redox imbalance. Since its formal recognition in 2012, ferroptosis has emerged as a central pathway linking metabolic stress and oxidative injury to both physiologic and pathologic processes. Its functions extend from tissue sculpting during embryogenesis and tumor suppression to pathologic contributions in neurodegeneration, cardiovascular disease, liver and kidney injury, cancer, and inflammatory disorders. Despite these advances in our understanding of ferroptosis, critical questions remain regarding its precise regulation, context-specific consequences, and interactions with other cell death pathways. Continued progress in identifying biomarkers, defining context-specific roles, and developing selective modulators will be essential to translate ferroptosis biology into clinical therapies with broad impact. Here, we describe the current state of our understanding of the role of ferroptosis in physiology and its potential as a target mechanism in heart and kidney disease.
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