ArticleDisease models & mechanisms2024
Promoting mitochondrial dynamics by inhibiting the PINK1-PRKN pathway to relieve diabetic nephropathy.
Article in Disease models & mechanisms, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 8 citations in OpenAlex.
- NSUN4-dependent m5C modification facilitates mitochondrial fission to accelerate diabetic nephropathy process via regulating SMURF1/CAMK1 axis.Clinical and translational medicine · 2026Article
- PTEN modulates mitochondrial dysfunction in podocytes via the PINK1/Parkin signal pathway.Translational pediatrics · 2026Article
- Mitochondrial Dynamics in Diabetic Kidney Disease: Underlying Mechanisms and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Modified Shen-Yan-Fang-Shuai formula attenuates diabetic kidney disease progression via regulation of HIF-1α-mediated mitochondrial energy metabolism.Chinese medicine · 2026Article
- Precision Nanomedicine for Renal Tubular Injury: From Passive Accumulation to Subcellular Targeting.International journal of nanomedicine · 2026Review
- Targeting Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs): A Novel Therapeutic Strategy for Diabetic Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Article
- Role of nuclear receptors, lipid metabolism, and mitochondrial function in the pathogenesis of diabetic kidney disease.American journal of physiology. Renal physiology · 2025Review
- Natural small molecules regulating the mitophagy pathway counteract the pathogenesis of diabetes and chronic complications.Frontiers in pharmacology · 2025Review
- [Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
- Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is a metabolic disorder characterized by high blood glucose levels and is a leading cause of kidney disease. Diabetic nephropathy has been attributed to dysfunctional mitochondria. However, many questions remain about the exact mechanism. The structure, function and molecular pathways are highly conserved between mammalian podocytes and Drosophila nephrocytes; therefore, we used flies on a high-sucrose diet to model type 2 diabetic nephropathy. The nephrocytes from flies on a high-sucrose diet showed a significant functional decline and decreased cell size, associated with a shortened lifespan. Structurally, the nephrocyte filtration structure, known as the slit diaphragm, was disorganized. At the cellular level, we found altered mitochondrial dynamics and dysfunctional mitochondria. Regulating mitochondrial dynamics by either genetic modification of the Pink1-Park (mammalian PINK1-PRKN) pathway or treatment with BGP-15, mitigated the mitochondrial defects and nephrocyte functional decline. These findings support a role for Pink1-Park-mediated mitophagy and associated control of mitochondrial dynamics in diabetic nephropathy, and demonstrate that targeting this pathway might provide therapeutic benefits for type 2 diabetic nephropathy.
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