ReviewCells2022
Mitochondrial Contribution to Inflammation in Diabetic Kidney Disease.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses 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
22 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Efficacy and safety of jinlida granule in the treatment of diabetic kidney disease: a systematic review and meta-analysis of randomized controlled trials.Frontiers in pharmacology · 2026Pooled it
- Association between remnant cholesterol and chronic kidney disease: Systematic review and meta-analysis.Diabetes, obesity & metabolism · 2025Pooled it
- USP18 Serves as a Key Mediator of cGAS-STING for Cardiac Aging in Diabetes.Cell biochemistry and function · 2026Article
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- Mechanisms of diabetic kidney disease and established and emerging treatments.Nature reviews. Endocrinology · 2026Review
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
- Integrative analysis of mitochondrial and immune pathways in diabetic kidney disease: identification of AASS and CASP3 as key predictors and therapeutic targets.Renal failure · 2025Article
- Dapagliflozin treatment ameliorates oxidative stress, apoptosis and inflammation in tenofovir-induced nephrotoxicity in rats.Scientific reports · 2025Article
- Role of nuclear receptors, lipid metabolism, and mitochondrial function in the pathogenesis of diabetic kidney disease.American journal of physiology. Renal physiology · 2025Review
- The role of lactate and lactylation in diabetic nephropathy.Molecular biology reports · 2025Review
- Control of Mitochondrial Quality: A Promising Target for Diabetic Kidney Disease Treatment.Kidney international reports · 2025Review
- Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NADAntioxidants (Basel, Switzerland) · 2025Review
- The Role of Mitochondria in Diabetic Kidney Disease and Potential Therapeutic Targets.Kidney international reports · 2025Review
- Unraveling the role of mitochondrial dysfunction in diabetic kidney disease: insights and interventions.Frontiers in pharmacology · 2025Review
- Protective effect of mesenchymal stromal cells in diabetic nephropathy: the In vitro and In vivo role of the M-Sec-tunneling nanotubes.Clinical science (London, England : 1979) · 2024Article
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- Article
- PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms.Molecular biology reports · 2024Review
- Transplantation: platform to study recurrence of disease.Frontiers in immunology · 2024Article
- Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases.Cell death & disease · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Diabetes is the leading cause of chronic kidney disease worldwide. Despite the burden, the factors contributing to the development and progression of diabetic kidney disease (DKD) remain to be fully elucidated. In recent years, increasing evidence suggests that mitochondrial dysfunction is a pathological mediator in DKD as the kidney is a highly metabolic organ rich in mitochondria. Furthermore, low grade chronic inflammation also contributes to the progression of DKD, and several inflammatory biomarkers have been reported as prognostic markers to risk-stratify patients for disease progression and all-cause mortality. Interestingly, the term "sterile inflammation" appears to be used in the context of DKD describing the development of intracellular inflammation in the absence of bacterial or viral pathogens. Therefore, a link between mitochondrial dysfunction and inflammation in DKD exists and is a hot topic in both basic research and clinical investigations. This review summarizes how mitochondria contribute to sterile inflammation in renal cells in DKD.
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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.