ArticleDiabetes2017
Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility.
Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 3 of them syntheses 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.
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Who cites it
168 citing papers in PubMed, 3 syntheses or guidelines pooled it, 254 citations in OpenAlex.
- Effects of continuous positive airway pressure on renal function in adults with obstructive sleep apnea: a systematic review and meta-analysis.Sleep & breathing = Schlaf & Atmung · 2025Pooled it
- The effect of liraglutide on renal function in type 2 diabetes: a meta-analysis of randomized controlled studies.African health sciences · 2022 · on this mapPooled it
- Mitochondrial Dysfunction in Individuals with Diabetic Kidney Disease: A Systematic Review.Cells · 2022Pooled it
- Long-Term Intensive Lifestyle Intervention Promotes Improvement of Stage III Diabetic Nephropathy.Medical science monitor : international medical journal of experimental and clinical research · 2019Trial
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- Review
- Canagliflozin Alleviates Diabetic Glomerular Endothelial Injury via Melibiose in a Microbiota-Dependent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Podocyte-derived endothelin-1 and endothelial cell endothelin A receptors are essential for glomerular injury in mouse models of focal segmental glomerulosclerosis.Kidney international · 2026Article
- Multiparametric MRI as predictors for evaluating renal ischemia reperfusion injury and protective effect of Mito-TEMPO in rat model.BMC nephrology · 2026Article
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Article
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- Mechanisms of diabetic kidney disease and established and emerging treatments.Nature reviews. Endocrinology · 2026Review
- cGAS-STING pathway in innate immunity and its cell-specific role in kidney diseases.Frontiers in immunology · 2026Review
- Targeting the TFAM-cGAS-STING axis: a mitochondrial-inflammatory link in the pathogenesis and treatment of diabetic kidney disease.International urology and nephrology · 2026Review
- miRNA in the Progression of Diabetic Kidney Disease: New Insight.International journal of molecular sciences · 2025Review
- Temporal glomerular gene expression dynamics during disease progression in a mouse model of hypertension-accelerated diabetic kidney disease.Animal models and experimental medicine · 2025Article
108 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
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The molecular signaling mechanisms between glomerular cell types during initiation/progression of diabetic kidney disease (DKD) remain poorly understood. We compared the early transcriptome profile between DKD-resistant C57BL/6J and DKD-susceptible DBA/2J (D2) glomeruli and demonstrated a significant downregulation of essential mitochondrial genes in glomeruli from diabetic D2 mice, but not in C57BL/6J, with comparable hyperglycemia. Diabetic D2 mice manifested increased mitochondrial DNA lesions (8-oxoguanine) exclusively localized to glomerular endothelial cells after 3 weeks of diabetes, and these accumulated over time in addition to increased urine secretion of 8-oxo-deoxyguanosine. Detailed assessment of glomerular capillaries from diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae. Glomerular endothelial mitochondrial dysfunction was associated with increased glomerular endothelin-1 receptor type A (Ednra) expression and increased circulating endothelin-1 (Edn1). Selective Ednra blockade or mitochondrial-targeted reactive oxygen species scavenging prevented mitochondrial oxidative stress of endothelial cells and ameliorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glomerulosclerosis. In human DKD, increased urine 8-oxo-deoxyguanosine was associated with rapid DKD progression, and biopsies from patients with DKD showed increased mitochondrial DNA damage associated with glomerular endothelial EDNRA expression. Our studies show that DKD susceptibility was linked to mitochondrial dysfunction, mediated largely by Edn1-Ednra in glomerular endothelial cells representing an early event in DKD progression, and suggest that cross talk between glomerular endothelial injury and podocytes leads to defects and depletion, albuminuria, and glomerulosclerosis.
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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.