ArticleKidney international reports2025
The Role of Mitochondrial AKT1 Signaling in Renal Tubular Injury of Metabolic Syndrome.
Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed.
- A tri-scale in silico framework integrating pharmacovigilance and mechanistic modeling suggests tepotinib-associated acute kidney injury risk.Renal failure · 2026Article
- Dual roles of renal tubular mitochondrial Akt1 in protecting against diabetic nephropathy and improving body glucose metabolism.The Journal of endocrinology · 2026Article
- Interpretable Machine Learning for Predicting Metabolic Syndrome-Kidney Stone Disease Comorbidity: The Role of Dietary Micronutrients.Food science & nutrition · 2026Article
- Mitochondrial Dysfunction at the Intersection of CKM Syndrome: Molecular Mechanisms and Path-to-Target Therapies.International journal of molecular sciences · 2026Review
- Ellagic Acid Prevents Obesity in High-Fat Diet-Fed Rats by Ameliorating Oxidative Stress via Modulation of the PPARG/STAT3/p-AKT1 Axis.Foods (Basel, Switzerland) · 2026Article
- An Exploratory Analysis of Potential Core Targets and Signaling Pathways Linking Dexmedetomidine to Diabetes Insipidus: Integration of FAERS Pharmacovigilance Data, Network Toxicology and Clinical Transcriptomics.Drug design, development and therapy · 2026Article
- Metabolic syndrome and kidney dysfunction: emerging molecular and cellular mechanisms at the metabolic-renal interface.Frontiers in endocrinology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Metabolic syndrome (MetS) is increasingly recognized as a contributor to kidney disease, yet the underlying mechanisms remain poorly defined. Recent studies suggest a pivotal role for mitochondrial dysfunction in renal injury. We hypothesized that mitochondrial AKT1 signaling in renal tubules plays a critical role in MetS-related kidney injuries. Methods: MetS was induced in a 8-week-old C57BL/6 male mice using a high-fat diet (HFD) for 4 months compared with controls on a standard chow diet. Additional experiments were conducted in DB/DB diabetic mice and their controls (WT and DB/WT) to validate findings. Renal metabolic parameters, mitochondrial AKT1 signaling, and markers of kidney injury were assessed. Results: MetS mice exhibited significant weight gain, altered glucose handling, and decreased energy expenditure. Although kidney size and basic renal function (blood urea nitrogen [BUN], creatinine) were unchanged, markers of renal damage, including proteinuria ( Conclusion: These findings underscore the mechanistic link between mitochondrial AKT1 signaling and renal tubular injury in MetS. Targeting mitochondrial dysfunction may offer new avenues for preventing and treating kidney diseases in patients with MetS.
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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 Socratic graph.