ReviewNature reviews. Nephrology2015
Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.
Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 549 papers.
What it found
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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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Who cites it
549 citing papers in PubMed, 825 citations in OpenAlex.
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury.Renal failure · 2026Article
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
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- Loss of Erbin in tubular epithelial cells sensitizes mice to acute kidney injury and aggravates renal fibrosis.The EMBO journal · 2026Article
- HNF4A maintains proximal tubule identity and limits injury-associated cell states in the adult mouse kidney.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Article
- A novel Keap1-Nrf2 inhibitor 6K delays the progression of AKI-to-CKD by mitigating maladaptive repair.Redox biology · 2026Article
- Tackling aging and chronic disease: How space exploration and the 'chameleon effect' of pharmaceuticals can lead the way.Experimental physiology · 2026Review
- Beyond the horizon: Why space biology is the next great innovation opportunity.Experimental physiology · 2026Article
- Review
- Renal Tubular Epithelial CRLF1 Interacts With ITGB1 to Accelerate Fibrosis During the Transition From AKI to CKD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- Targeting YAP1-Mediated Tubular Cell Senescence to Attenuate Maladaptive Repair and Fibrotic Transition After Acute Kidney Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cellular senescence in kidney diseases: a bibliometric analysis of global trends, knowledge bases, and emerging therapeutic frontiers.International urology and nephrology · 2026Article
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- Pharmacologic disruption of HuR-RNA interactions prevents maladaptive tubular repair and AKI-to-CKD progression.American journal of physiology. Renal physiology · 2026Article
- Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease.Nature reviews. Nephrology · 2026Review
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- Immunosenescence in systemic and multi-organ aging: mechanisms, inter-organ crosstalk, and translational opportunities.npj aging · 2026Review
489 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.