ReviewJournal of the American Society of Nephrology : JASN2019
Mitochondria in Sepsis-Induced AKI.
Review in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
145 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Machine learning for the prediction of mortality in patients with sepsis-associated acute kidney injury: a systematic review and meta-analysis.BMC infectious diseases · 2024Pooled it
- Research hotspots and future trends in sepsis-associated acute kidney injury: a bibliometric and visualization analysis.Frontiers in medicine · 2024Pooled it
- Explainable machine learning using urinary metabolomics to predict pediatric sepsis-associated acute kidney injury: a two-center prospective observational study.Renal failure · 2026Observational
- An NLRP3 inflammasome-anchored Astragalus mechanistic prior yields a mortality-associated transcriptomic signal in ICU sepsis: a secondary analysis with exploratory cross-cohort assessment.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- α7nAChR agonist GTS-21 ameliorates sepsis-induced acute kidney injury via MEF2/PGC-1α/HO-1 axis in mice.Clinical and translational medicine · 2026Article
- Article
- GATM alleviates sepsis-induced acute kidney injury via PDK4-mediated glycolytic reprogramming in renal tubular epithelial cells.Cellular and molecular life sciences : CMLS · 2026Article
- Supervised machine learning models for predicting sepsis-associated acute kidney injury in children: a real-world evaluation.World journal of pediatrics : WJP · 2026Article
- SUMOylation protects against sepsis-associated acute kidney injury by stabilizing IκBα.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics.Biomedicines · 2026Review
- Relationship between urine output and 28-day mortality in patients with acute kidney injury receiving continuous renal replacement therapy.BMC nephrology · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Sirtuin 4 Knockout Aggravates Sepsis-Induced Acute Liver Injury by Enhancing Mitochondrial Fission and Mitophagy in Hepatocytes.Mediators of inflammation · 2026Article
- Evaluating the Diagnostic Value and Molecular Mechanism of Energy Metabolism-Related Gene PEA15 in Sepsis.Journal of inflammation research · 2026Article
- Mechanisms of salvianolic acids in kidney disease therapy: advances and perspectives.Frontiers in pharmacology · 2026Review
- CX3CL1 deficiency ameliorates acute kidney injury by inhibiting macrophage mitochondrial dysfunction and mtDNA-cGAS-STING signaling.Cell death discovery · 2025Article
- Mitochondrial immunometabolism in sepsis: orchestrating macrophage polarization and dysfunction.European journal of medical research · 2025Review
- Integrated single-cell and clinical transcriptomic analysis identifies blunted glycolytic activation as a hallmark of maladaptive repair in renal ischemia-reperfusion.Renal failure · 2025Article
- Integrated multi-omics of mitophagy-related molecular subtype characterization and biomarker identification in sepsis.Scientific reports · 2025Article
- Baicalin alleviates sepsis-associated acute kidney injury through activation of the PPAR-γ/UCP1 signaling pathway.Renal failure · 2025Article
85 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKI is a common clinical condition associated with the risk of developing CKD and ESKD. Sepsis is the leading cause of AKI in the intensive care unit (ICU) and accounts for nearly half of all AKI events. Patients with AKI who require dialysis have an unacceptably high mortality rate of 60%-80%. During sepsis, endothelial activation, increased microvascular permeability, changes in regional blood flow distribution with resulting areas of hypoperfusion, and hypoxemia can lead to AKI. No effective drugs to prevent or treat human sepsis-induced AKI are currently available. Recent research has identified dysfunction in energy metabolism as a critical contributor to the pathogenesis of AKI. Mitochondria, the center of energy metabolism, are increasingly recognized to be involved in the pathophysiology of sepsis-induced AKI and mitochondria could serve as a potential therapeutic target. In this review, we summarize the potential role of mitochondria in sepsis-induced AKI and identify future therapeutic approaches that target mitochondrial function in an effort to treat sepsis-induced 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 OpenQuestion graph.