ReviewInternational journal of molecular sciences2025
Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- REDD1 deficiency alleviates podocyte PANoptosis and restores autophagy in diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- α-Synuclein as a molecular link between Parkinson's disease and chronic kidney disease: insights into the kidney-brain axis.Metabolic brain disease · 2026Review
- Mechanism of action and clinical application of autophagy in multiple sclerosis (Review).International journal of molecular medicine · 2026Review
- Targeting PSAT1 in diabetic kidney disease: a ferroptosis-driven strategy for precision therapy.Molecular and cellular biochemistry · 2026Article
- Metabolic Dysfunction-associated Steatotic Liver Disease and Chronic Kidney Disease: From Epidemiology and Pathophysiology to Clinical Prediction and Treatment Options.Journal of clinical and translational hepatology · 2026Review
- Adipokine networks in diabetic kidney disease: mechanistic insights and therapeutic implications.Lipids in health and disease · 2026Review
- Polyphyllin II attenuates renal fibrosis in diabetic kidney disease partly through regulation of autophagy and PI3K/AKT/mTOR signaling.Frontiers in pharmacology · 2026Article
- C3a/C3aR axis is involved in diabetic kidney injury by regulating podocyte mitophagy in diabetic nephropathy.International journal of molecular medicine · 2025Article
- IJMS Special Issue-Molecular Mechanisms of Diabetic Kidney Disease 2.0.International journal of molecular sciences · 2025Article
- Inflammatory mechanisms in diabetic nephropathy: emerging insights and targeted therapeutics.Frontiers in medicine · 2025Review
- Role of Metabolic Abnormalities During the Progression of Chronic Kidney Disease and Preventive Strategies.International journal of medical sciences · 2025Review
- Lysine Methyltransferases SMYD2 and SMYD3: Emerging Targets in Kidney Diseases.Kidney diseases (Basel, Switzerland)Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy and mitophagy are critical cellular processes that maintain homeostasis by removing damaged organelles and promoting cellular survival under stress conditions. In the context of diabetic kidney disease, these mechanisms play essential roles in mitigating cellular damage. This review provides an in-depth analysis of the recent literature on the relationship between autophagy, mitophagy, and diabetic kidney disease, highlighting the current state of knowledge, existing research gaps, and potential areas for future investigations. Diabetic nephropathy (DN) is traditionally defined as a specific form of kidney disease caused by long-standing diabetes, characterized by the classic histological lesions in the kidney, including mesangial expansion, glomerular basement membrane thickening, nodular glomerulosclerosis (Kimmelstiel-Wilson nodules), and podocyte injury. Clinical markers for DN are albuminuria and the gradual decline in glomerular filtration rate (GFR). Diabetic kidney disease (DKD) is a broader and more inclusive term, for all forms of chronic kidney disease (CKD) in individuals with diabetes, regardless of the underlying pathology. This includes patients who may have diabetes-associated kidney damage without the typical histological findings of diabetic nephropathy. It also accounts for patients with other coexisting kidney diseases (e.g., hypertensive nephrosclerosis, ischemic nephropathy, tubulointerstitial nephropathies), even in the absence of albuminuria, such as a reduction in GFR.
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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.