ReviewCell death discovery2024
Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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
61 citing papers in PubMed, 69 citations in OpenAlex.
- Biomimetic nanocages with cascade homing for theranostics of ischemia-reperfusion acute kidney injury.Materials today. Bio · 2026Article
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Melanocortin 1 Receptor Signaling Protects Against Tubular Epithelial Cell Injury and M1 Macrophage Polarization in Acute Kidney Injury.Integrative zoology · 2026Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Connexin 43-dependent mesenchymal stem cell mitochondrial transfer activates PGC1α disrupting oxidative-inflammation axis in ischemia-reperfusion injury.Signal transduction and targeted therapy · 2026Article
- The Estrogen-Mitochondria Axis in Bipolar Disorder: From Fluctuating Hormones to Failing Bioenergetics.Biological psychiatry global open science · 2026Review
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Combined morphologic and immunohistochemical assessment of KIM-1-positive proximal tubular vacuolation in one-hour kidney allograft biopsies.BMC nephrology · 2026Article
- Novel interactions between the C5-C5aR1 Axis and IF1: Implications for kidney mitochondrial physiology and ischemia-reperfusion injury.Physiological reports · 2026Article
- Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.Journal of nanobiotechnology · 2026Review
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- The aging eye: navigating molecular mechanisms and innovative interventions.Biogerontology · 2026Review
- Identification and functional validation of mitochondria-related genes associated with tubular injury in kidney transplantation and ischemia-reperfusion injury.Biology direct · 2026Article
- Renal-targeted tFNA-TPP nanoagonist treats acute kidney injury by amplifying mitophagy.Materials today. Bio · 2026Article
- [Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Selenoprotein GPX3 regulates NADPH oxidase expression by inhibiting the MAPK signaling pathway and thereby attenuating the inflammatory response in renal ischemia-reperfusion injury.Genes & diseases · 2026Article
- Mitigation of Ischemia/Reperfusion-Induced Acute Kidney Injury by Canagliflozin Is Associated with Altered Mitochondrial Dynamics and Reduced Proliferation in Swine.Biomolecules · 2026Article
- Research progress of nanoparticles in the diagnosis and treatment of renal ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Review
1 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
7 authors at 1 institution in 1 country.
Funding
Abstract
Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The kidney is susceptible to IRI under several clinical conditions, including hypotension, sepsis, and surgical procedures, such as partial nephrectomy and kidney transplantation. Extensive research has been conducted on the mechanism and intervention strategies of renal IRI in past decades; however, the complex pathophysiology of IRI-induced AKI (IRI-AKI) is not fully understood, and there remains a lack of effective treatments for AKI. Renal IRI involves several processes, including reactive oxygen species (ROS) production, inflammation, and apoptosis. Mitochondria, the centers of energy metabolism, are increasingly recognized as substantial contributors to the early phases of IRI. Multiple mitochondrial lesions have been observed in the renal tubular epithelial cells (TECs) of IRI-AKI mice, and damaged or dysfunctional mitochondria are toxic to the cells because they produce ROS and release cell death factors, resulting in TEC apoptosis. In this review, we summarize the recent advances in the mitochondrial pathology in ischemic AKI and highlight promising therapeutic approaches targeting mitochondrial dysfunction to prevent or treat human ischemic AKI.
Identifiers
What OpenQuestion 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 OpenQuestion graph.