ReviewJournal of the American Society of Nephrology : JASN2014
Regulated cell death in AKI.
Review in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
322 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of resveratrol on renal ischemia-reperfusion injury: A systematic review and meta-analysis.Frontiers in nutrition · 2022Pooled it
- Transcriptome and weighted gene co-expression network analysis identify hub genes and pathways in rat kidneys after deep hypothermic circulatory arrest.Renal failure · 2026Article
- Loss of Erbin in tubular epithelial cells sensitizes mice to acute kidney injury and aggravates renal fibrosis.The EMBO journal · 2026Article
- Targeting iRhom2-mediated PANoptosis ameliorates acute kidney injury.Acta pharmacologica Sinica · 2026Article
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- Microvascular autophagy and caspase-3 activation are central regulators of renal fibrosis after ischemia-reperfusion.JCI insight · 2026Article
- Magnesium as a Bioenergetic Checkpoint Linking Mitochondrial Function, Metabolic Disease, and Aging.Aging cell · 2026Review
- The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury.Current therapeutic research, clinical and experimental · 2026Article
- ELMO1 dependent efferocytosis protects from nephrotoxin induced acute kidney injury.Cell death discovery · 2026Article
- Unraveling the therapeutic potential of luteolin in renal pathology: a comprehensive pathway oriented approach.Pharmacological reports : PR · 2026Review
- Article
- STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury.Cell communication and signaling : CCS · 2026Article
- PPARγ agonism ameliorates acute kidney injury by inhibiting neutrophil extracellular trap formation-mediated renal tubular epithelial cell PANoptosis.Cell communication and signaling : CCS · 2026Article
- Keratin 20 Suppresses Exosomal Secretion of Peroxiredoxin 2 and Ferroptosis in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Article
- Function of molecular-weight-optimized Astragalus polysaccharides in cisplatin-caused acute kidney injury: mechanisms centered on gut microbiota regulation and precise treatment approaches.Frontiers in microbiology · 2026Review
- Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.International journal of biological sciences · 2026Article
- Improved bioavailability and anti-nephrotoxicity efficacy of polydatin on cisplatin-induced AKIInternational journal of pharmaceutics: X · 2025Article
- Acute kidney injury and iron metabolism: A narrative review focusing on pathophysiology and therapy.Smart molecules : open access · 2025Review
- Glycyrrhizin alleviates contrast-induced acute kidney injury via inhibiting HMGB1-mediated renal tubular epithelial cells ferroptosis.Renal failure · 2025Article
- Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Review
262 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
6 authors.
Funding
Abstract
AKI is pathologically characterized by sublethal and lethal damage of renal tubules. Under these conditions, renal tubular cell death may occur by regulated necrosis (RN) or apoptosis. In the last two decades, tubular apoptosis has been shown in preclinical models and some clinical samples from patients with AKI. Mechanistically, apoptotic cell death in AKI may result from well described extrinsic and intrinsic pathways as well as ER stress. Central converging nodes of these pathways are mitochondria, which become fragmented and sensitized to membrane permeabilization in response to cellular stress, resulting in the release of cell death-inducing factors. Whereas apoptosis is known to be regulated, tubular necrosis was thought to occur by accident until recent work unveiled several RN subroutines, most prominently receptor-interacting protein kinase-dependent necroptosis and RN induced by mitochondrial permeability transition. Additionally, other cell death pathways, like pyroptosis and ferroptosis, may also be of pathophysiologic relevance in AKI. Combination therapy targeting multiple cell-death pathways may, therefore, provide maximal therapeutic benefits.
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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.