ArticleThe Journal of clinical investigation2011
PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 papers, 1 of them a synthesis that pooled it.
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
326 citing papers in PubMed, 1 synthesis or guideline pooled it, 495 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- IgA nephropathy is associated with elevated urinary mitochondrial DNA copy numbers.Scientific reports · 2019Trial
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- A mitochondria-targeted HRedox biology · 2026Article
- Inhibition of TGF-β in Tubule Cells Increases Respiration via Upregulation of Respiratory Genes.Tissue engineering. Part A · 2026Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Selenoprotein H targets MTCH2 to regulate MFN2-dependent mitochondrial quality control to alleviate acute kidney injury.Journal of advanced research · 2026Article
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Magnesium as a Bioenergetic Checkpoint Linking Mitochondrial Function, Metabolic Disease, and Aging.Aging cell · 2026Review
- Pseudogene-Derived Long Noncoding RNAs GSTM3P1/Gstm2-ps1 Exacerbate Sepsis-Associated Acute Kidney Injury by Suppressing Their Parent Gene Translation.The American journal of pathology · 2026Article
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
- Lipids in kidney diseases: from systemic imbalance to intrarenal alterations of cellular lipid metabolism in rare and common kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Special Issue: "Molecular Mechanisms and Regulation in Chronic Kidney Diseases".International journal of molecular sciences · 2026Article
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- Metabolic syndrome and kidney dysfunction: emerging molecular and cellular mechanisms at the metabolic-renal interface.Frontiers in endocrinology · 2026Review
- Modulation of mitochondrial quality control in sepsis by traditional Chinese medicine: mechanistic insights and translational perspectives.Frontiers in pharmacology · 2026Review
- Mitochondria - an old-new link in the progression of renal disease.Renal failure · 2025Article
- Integrated single-cell and clinical transcriptomic analysis identifies blunted glycolytic activation as a hallmark of maladaptive repair in renal ischemia-reperfusion.Renal failure · 2025Article
266 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
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Sepsis-associated acute kidney injury (AKI) is a common and morbid condition that is distinguishable from typical ischemic renal injury by its paucity of tubular cell death. The mechanisms underlying renal dysfunction in individuals with sepsis-associated AKI are therefore less clear. Here we have shown that endotoxemia reduces oxygen delivery to the kidney, without changing tissue oxygen levels, suggesting reduced oxygen consumption by the kidney cells. Tubular mitochondria were swollen, and their function was impaired. Expression profiling showed that oxidative phosphorylation genes were selectively suppressed during sepsis-associated AKI and reactivated when global function was normalized. PPARγ coactivator-1α (PGC-1α), a major regulator of mitochondrial biogenesis and metabolism, not only followed this pattern but was proportionally suppressed with the degree of renal impairment. Furthermore, tubular cells had reduced PGC-1α expression and oxygen consumption in response to TNF-α; however, excess PGC-1α reversed the latter effect. Both global and tubule-specific PGC-1α-knockout mice had normal basal renal function but suffered persistent injury following endotoxemia. Our results demonstrate what we believe to be a novel mechanism for sepsis-associated AKI and suggest that PGC-1α induction may be necessary for recovery from this disorder, identifying a potential new target for future therapeutic studies.
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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.