ReviewAmerican journal of physiology. Renal physiology2024
Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.
Review in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The molecular mechanism of cuproptosis and research progress in pancreatic diseases.Annals of medicine · 2026Pooled it
- Morin attenuates vancomycin-induced nephrotoxicity via Nrf-2/HO-1, SIRT1/PGC1α and AKT/FOXO1A pathways.Molecular biology reports · 2026Article
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- Research Progress on the Treatment of Renal Injury with Esculetin: Multi-Target Pharmacological Mechanism and Clinical Translation Prospect.International journal of molecular sciences · 2026Review
- Lipid Peroxidation in Cancer Therapy: Molecular Mechanisms Involving Oxidative Stress, Cell Death, and Therapeutic Response.Molecules (Basel, Switzerland) · 2026Review
- Article
- Modulating regulated cell death: mechanistic insights into traditional Chinese medicine metabolites for ischemia/reperfusion-induced acute kidney injury.Frontiers in pharmacology · 2026Review
- Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling.Journal of ginseng research · 2026Article
- A multi-omics landscape of programmed cell death in acetaminophen-induced acute kidney injury.Renal failure · 2025Article
- Persistent subclinical renal injury in female rats following renal ischemia-reperfusion injury.Clinical science (London, England : 1979) · 2025Article
- NLRP3 Inflammasome-Mediated Pyroptosis in Diabetic Nephropathy: Pathogenic Mechanisms and Therapeutic Targets.Journal of inflammation research · 2025Review
- Nutritional management of pediatric nephrotic syndrome regarding oxidative stress and antioxidant balance.Frontiers in immunology · 2025Review
- Paraptosis-A Distinct Pathway to Cell Death.International journal of molecular sciences · 2024Review
- The Effect of Low-Density Lipoprotein Receptor-Related Protein-1 on Acute Kidney Injury and Renal Tubular Epithelial Triglyceride Accumulation.Kidney diseases (Basel, Switzerland)Article
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
The involvement of cell death in acute kidney injury (AKI) is linked to multiple factors including energy depletion, electrolyte imbalance, reactive oxygen species, inflammation, mitochondrial dysfunction, and activation of several cell death pathway components. Since our review in 2003, discussing the relative contributions of apoptosis and necrosis, several other forms of cell death have been identified and are shown to contribute to AKI. Currently, these various forms of cell death can be fundamentally divided into accidental cell death and regulated or programmed cell death based on functional aspects. Several death initiator and effector molecules switch molecules that may act as signaling components triggering either death or protective mechanisms or alternate cell death pathways have been identified as part of the machinery. Intriguingly, several of these cell death pathways share components and signaling pathways suggesting complementary or compensatory functions. Thus, defining the cross talk between distinct cell death pathways and identifying the unique molecular effectors for each type of cell death may be required to develop novel strategies to prevent cell death. Furthermore, depending on the multiple forms of cell death simultaneously induced in different AKI settings, strategies for combination therapies that block multiple cell death pathways need to be developed to completely prevent injury, cell death, and renal function. This review highlights the various cell death pathways, cross talk, and interactions between different cell death modalities in AKI.
Indexed as
Identifiers
What Socratic 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 Socratic graph.