ReviewFrontiers in medicine2022
Programmed Cell Death in Sepsis Associated Acute Kidney Injury.
Review in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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
56 citing papers in PubMed, 82 citations in OpenAlex.
- The impact of ulinastatin on lymphocyte apoptosis and autophagy in sepsis patients.Scientific reports · 2024Trial
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Article
- Knockdown of PTEN Inhibits Autophagy-Dependent Ferroptosis to Alleviate LPS-Induced Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Article
- Pomiferin protects against sepsis-associated acute liver and kidney injury via inhibition of NF-κB activation, oxidative stress, and cytochrome-c.Scientific reports · 2026Article
- Protective Effects of Opuntiol on Lipopolysaccharide-Induced Acute Kidney Injury in Mice.Physiological research · 2026Article
- Serum HDAC3 as an early biomarker for prediction and staging of sepsis-associated AKI: prospective cohort study.BMC infectious diseases · 2026Article
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Impact of Melatonin on Sepsis-Associated Acute Kidney Injury in Rat Model of Lipopolysaccharide Endotoxemia.Current issues in molecular biology · 2026Article
- Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis.Chinese medicine · 2026Article
- NTN1 regulates autophagy through the MAP1B/DAPK1 axis to ameliorate acute kidney injuryOpen medicine (Warsaw, Poland) · 2026Article
- Source-stratified gut-extraintestinal organ crosstalk in sepsis-associated acute gastrointestinal injury and paralytic ileus: the gut as both driver and target.Frontiers in medicine · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Gut microbiota and sepsis-associated acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
- METTL1 aggravates sepsis-acute kidney injury by promoting mHistology and histopathology · 2025Article
- Vitamin D receptor modulates autophagy via miR-20a-5p/ATG16L1 axis to alleviate lipopolysaccharide-induced acute kidney injury.Renal failure · 2025Article
- Mitochondrial Quality Control and Cell Death.International journal of molecular sciences · 2025Review
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated acute kidney injury (SA-AKI) is common in patients with severe sepsis, and has a high incidence rate and high mortality rate in ICU patients. Most patients progress to AKI before drug treatment is initiated. Early studies suggest that the main mechanism of SA-AKI is that sepsis leads to vasodilation, hypotension and shock, resulting in insufficient renal blood perfusion, finally leading to renal tubular cell ischemia and necrosis. Research results in recent years have shown that programmed cell death such as apoptosis, necroptosis, pyroptosis and autophagy play important roles. In the early stage of sepsis-related AKI, autophagy bodies form and inhibit various types of programmed cell death. With the progress of disease, programmed cell death begins. Apoptosis promoter represents caspase-8-induced apoptosis and apoptosis effector represents caspase-3-induced apoptosis, however, caspase-11 and caspase-1 regulate gasdermin D-mediated pyroptosis. Caspase-8 and receptor interacting kinase 1 bodies mediate necroptosis. This review focuses on the pathophysiological mechanisms of various programmed cell death in sepsis-related AKI.
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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 Socratic graph.