ArticleNeurobiology of disease2014
PGC-1α regulation of mitochondrial degeneration in experimental diabetic neuropathy.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 93 citations in OpenAlex.
- Selective inhibition of monoamine oxidase B represents a therapeutic strategy for diabetic peripheral neuropathy.Acta pharmacologica Sinica · 2026Article
- Focused Ultrasound Modulation of PGC-1α Pathways in Neurological Disease: Mechanistic Rationale and Translational Opportunities.Molecular neurobiology · 2026Review
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- A novel extracellular flux assay workflow uncovers impaired sciatic nerve mitochondrial respiration in diabetic db/db mice.Cell communication and signaling : CCS · 2026Article
- Glabridin as a selective Kv2.1 inhibitor ameliorates DPN pathology by disrupting the Aβ/Kv2.1/JNK/NF-κB/NLRP3/p-Tau pathway.Acta pharmacologica Sinica · 2025Article
- Mitochondrial dynamics in diabetic peripheral neuropathy: Pathogenesis, progression, and therapeutic approaches.Medicine · 2025Review
- Effect of high-dose N-acetyl cysteine on the clinical outcome of patients with diabetic peripheral neuropathy: a randomized controlled study.Diabetology & metabolic syndrome · 2025Article
- Administration of AICAR, an AMPK Activator, Prevents and Reverses Diabetic Polyneuropathy (DPN) by Regulating Mitophagy.International journal of molecular sciences · 2024Article
- Dimethyl fumarate improves nuclear factor erythroid-related factor 2-mediated antioxidant response to ameliorate functional and molecular deficits in experimental diabetic neuropathy.Indian journal of pharmacology · 2024Article
- Mitochondrial Dysfunction in Systemic Lupus Erythematosus: Insights and Therapeutic Potential.Diseases (Basel, Switzerland) · 2024Review
- Diabetic neuropathy: A NRF2 disease?Journal of diabetes · 2024Review
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- Targeted metabolomics reveals the aberrant energy status in diabetic peripheral neuropathy and the neuroprotective mechanism of traditional Chinese medicine JinMaiTong.Journal of pharmaceutical analysis · 2024Article
- NADInternational journal of molecular sciences · 2024Article
- Vincamine as an agonist of G-protein-coupled receptor 40 effectively ameliorates diabetic peripheral neuropathy in mice.Acta pharmacologica Sinica · 2023Article
- Alterations in Mitochondrial Morphology and Quality Control in Primary Mouse Lung Microvascular Endothelial Cells and Human Dermal Fibroblasts under Hyperglycemic Conditions.International journal of molecular sciences · 2023Article
- Sirtuins: Promising Therapeutic Targets to Treat Ischemic Stroke.Biomolecules · 2023Review
- The mActa diabetologica · 2023Article
- PGC1α: an emerging therapeutic target for chemotherapy-induced peripheral neuropathy.Therapeutic advances in neurological disorders · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial degeneration is considered to play an important role in the development of diabetic peripheral neuropathy in humans. Mitochondrial degeneration and the corresponding protein regulation associated with the degeneration were studied in an animal model of diabetic neuropathy. PGC-1α and its-regulated transcription factors including TFAM and NRF1, which are master regulators of mitochondrial biogenesis, are significantly downregulated in streptozotocin diabetic dorsal root ganglion (DRG) neurons. Diabetic mice develop peripheral neuropathy, loss of mitochondria, decreased mitochondrial DNA content and increased protein oxidation. Importantly, this phenotype is exacerbated in PGC-1α (-/-) diabetic mice, which develop a more severe neuropathy with reduced mitochondrial DNA and a further increase in protein oxidation. PGC-1α (-/-) diabetic mice develop an increase in total cholesterol and triglycerides, and a decrease in TFAM and NRF1 protein levels. Loss of PGC-1α causes severe mitochondrial degeneration with vacuolization in DRG neurons, coupled with reduced state 3 and 4 respiration, reduced expression of oxidative stress response genes and an increase in protein oxidation. In contrast, overexpression of PGC-1α in cultured adult mouse neurons prevents oxidative stress associated with increased glucose levels. The study provides new insights into the role of PGC-1α in mitochondrial regeneration in peripheral neurons and suggests that therapeutic modulation of PGC-1α function may be an attractive approach for treatment of diabetic neuropathy.
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