ReviewJournal of the American Society of Nephrology : JASN2016
Necroinflammation in Kidney Disease.
Review in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
What it found
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Who cites it
125 citing papers in PubMed.
- An HRedox biology · 2026Article
- SLC38A6 expression in renal tubular cells accelerates cisplatin-induced acute kidney injury by promoting cell apoptosis.The FEBS journal · 2026Article
- Pharmacologic disruption of HuR-RNA interactions prevents maladaptive tubular repair and AKI-to-CKD progression.American journal of physiology. Renal physiology · 2026Article
- Cholinergic stimulation after acute myocardial infarction improves hemodynamic parameters and modulates the renal injury in spontaneously hypertensive rats.Scientific reports · 2026Article
- Natural compounds targeting inflammatory signaling and cell adhesion molecules in ischemic acute kidney injury.Archives of pharmacal research · 2026Review
- Nano-Cilostazol Mitigates Cisplatin-Induced Nephrotoxicity in Rats via Modulation of Oxidative Stress, Apoptosis, Pyroptosis, and miRNA-155 Signaling.Antioxidants (Basel, Switzerland) · 2026Article
- A double-edged sword: the role of macrophage pyroptosis-driven cytokine storm-mediated intercellular communication in tumor progression.Frontiers in immunology · 2026Review
- Programmed cell death in gouty nephropathy: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- A machine learning-based model for predicting the postoperative risk of acute kidney injury in neonates.Translational pediatrics · 2025Article
- The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.Renal failure · 2025Review
- Article
- Hydrogen Sulfide Attenuates Cisplatin-Induced Acute Kidney Injury via Dual Inhibition of Apoptosis and Pyroptosis.Biomedicines · 2025Article
- Sex Differences in the Initiation and Progression of Necroptosis Following Kidney Ischemia-Reperfusion Injury.Biomedicines · 2025Article
- State of the art: Renal recovery after AKI - from basic science to clinical practice.Intensive care medicine · 2025Review
- Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025Review
- Molecular insights and clinical implications of DNA methylation in sepsis-associated acute kidney injury: a narrative review.BMC nephrology · 2025Review
- Article
- Targeting Hsp90α to inhibit HMGB1-mediated renal inflammation and fibrosis.Cell proliferation · 2025Article
65 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bidirectional causality between kidney injury and inflammation remains an area of unexpected discoveries. The last decade unraveled the molecular mechanisms of sterile inflammation, which established danger signaling via pattern recognition receptors as a new concept of kidney injury-related inflammation. In contrast, renal cell necrosis remained considered a passive process executed either by the complement-related membrane attack complex, exotoxins, or cytotoxic T cells. Accumulating data now suggest that renal cell necrosis is a genetically determined and regulated process involving specific outside-in signaling pathways. These findings support a unifying theory in which kidney injury and inflammation are reciprocally enhanced in an autoamplification loop, referred to here as necroinflammation. This integrated concept is of potential clinical importance because it offers numerous innovative molecular targets for limiting kidney injury by blocking cell death, inflammation, or both. Here, the contribution of necroinflammation to AKI is discussed in thrombotic microangiopathies, necrotizing and crescentic GN, acute tubular necrosis, and infective pyelonephritis or sepsis. Potential new avenues are further discussed for abrogating necroinflammation-related kidney injury, and questions and strategies are listed for further exploration in this evolving field.
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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.