ArticleeLife2021
Ferroptotic stress promotes the accumulation of pro-inflammatory proximal tubular cells in maladaptive renal repair.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 138 citations in OpenAlex.
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Lean adipocyte oxylipin signaling restrains breast cancer through ferroptosis.Science (New York, N.Y.) · 2026Article
- Synchronization of the 12-h circatidal rhythm maintains the kidney through repeated cycles of warm reperfusion in the hibernating ground squirrel.Function (Oxford, England) · 2026Article
- Article
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cellular microenvironment of erythropoietin-producing cells in hypoxic and injured mouse kidneys.Experimental physiology · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- The mtDNA-cGAS-STING Axis in Acute Kidney Injury and Maladaptive Repair: Preclinical Evidence for Traditional Chinese Medicine and Natural Product-Based Interventions.Journal of inflammation research · 2026Review
- Integrative analysis of cuproptosis in kidney ischemia-reperfusion injury: biomarker discovery and diagnostic model construction.Frontiers in molecular biosciences · 2026Article
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- A Balancing Act in Corneal Epithelial Repair: A MAPK-JUN/EGR1/TFAP2A Network Regulates Ferroptotic Cell Fate.International journal of general medicine · 2026Article
- Keratin 20 Suppresses Exosomal Secretion of Peroxiredoxin 2 and Ferroptosis in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Article
- Ferroptosis and renal fibrosis: mechanistic insights and emerging therapeutic targets.Renal failure · 2025Review
- Aging Mediates Inflammatory Transformation of Kidney-Resident Macrophages via Thrombospondin-1 Signaling.Immune network · 2025Article
- NSD1-916aa encoded by CircNSD1 contributes to AKI-to-CKD transition through inducing ferroptosis in tubular epithelial cells.JCI insight · 2025Article
- Integration of spatial protein imaging and transcriptomics in the human kidney tracks the regenerative potential of proximal tubules.Science advances · 2025Article
- Normothermic human kidney preservation drives iron accumulation and ferroptosis.Nature communications · 2025Article
- Altered renal vascular patterning reduces ischemic kidney injury and limits age-associated vascular loss.American journal of physiology. Renal physiology · 2025Article
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Overwhelming lipid peroxidation induces ferroptotic stress and ferroptosis, a non-apoptotic form of regulated cell death that has been implicated in maladaptive renal repair in mice and humans. Using single-cell transcriptomic and mouse genetic approaches, we show that proximal tubular (PT) cells develop a molecularly distinct, pro-inflammatory state following injury. While these inflammatory PT cells transiently appear after mild injury and return to their original state without inducing fibrosis, after severe injury they accumulate and contribute to persistent inflammation. This transient inflammatory PT state significantly downregulates glutathione metabolism genes, making the cells vulnerable to ferroptotic stress. Genetic induction of high ferroptotic stress in these cells after mild injury leads to the accumulation of the inflammatory PT cells, enhancing inflammation and fibrosis. Our study broadens the roles of ferroptotic stress from being a trigger of regulated cell death to include the promotion and accumulation of proinflammatory cells that underlie maladaptive repair.
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Registered trials
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