ArticleBioengineered2022
miR-188-3p abolishes germacrone-mediated podocyte protection in a mouse model of diabetic nephropathy in type I diabetes through triggering mitochondrial injury.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- Integrated 16S rRNA sequencing and metabolomic analysis reveals the potential protective mechanism of Germacrone on diabetic nephropathy in mice.Acta biochimica et biophysica Sinica · 2024Article
- Circular RNA 0016142 Knockdown Induces Ferroptosis in Hepatocellular Carcinoma Cells via Modulation of the MicroRNA-188-3p/Glutathione Peroxidase 4 Axis.Biochemical genetics · 2024Article
- Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway.Renal failure · 2023Article
- Mining Xanthine Oxidase Inhibitors from an Edible SeaweedMarine drugs · 2023Article
- Ferroptosis in diabetic nephropathy: Mechanisms and therapeutic implications.Metabolism open · 2023Review
- Ferroptosis: a new strategy for Chinese herbal medicine treatment of diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Astragaloside IV improves renal function and alleviates renal damage and inflammation in rats with chronic glomerulonephritis.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Neurotrophic Role of the Next-Generation Probiotic StrainNutrients · 2022Article
- Triptolide inhibits oxidative stress and inflammation via the microRNA-155-5p/brain-derived neurotrophic factor to reduce podocyte injury in mice with diabetic nephropathy.Bioengineered · 2022Article
- Liraglutide attenuates hepatic iron levels and ferroptosis in db/db mice.Bioengineered · 2022Article
- Alpiniae oxyphylla fructus extract promotes longevity and stress resistance ofFrontiers in pharmacology · 2022Article
- Canagliflozin mitigates ferroptosis and improves myocardial oxidative stress in mice with diabetic cardiomyopathy.Frontiers in endocrinology · 2022Article
Corrections and comments
- Retraction · 2024-02-20Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial injury-triggered podocyte apoptosis is a major risk factor for diabetic nephropathy (DN). However, the detailed relationship between mitochondrial homeostasis and podocyte apoptosis remains unclear. The present study aimed to explore the role and functional mechanism of germacrone in DN in type I diabetes (type I DN). A mouse model of type I DN was established by injecting streptozocin, and a podocyte injury model was constructed using high glucose (HG) induction. Histopathology was detected by hematoxylin and eosin and periodic acid-Schiff staining. Transmission electron microscopy and flow cytometry were used to evaluate the mitochondrial function. Germacrone simultaneously reduced blood glucose, 24 h proteinuria, and other nephrotic symptoms in a type 1 DN mouse model. Moreover, germacrone protected against mitochondrial damage, limited reactive oxygen species (ROS) accumulation, and restored glutathione peroxidase (GPX) activity and GPX4 protein expression, subsequently preventing podocyte apoptosis. Mechanistically, the increased miR-188-3p expression in type I DN mice was reversed in germacrone-challenged DN mice. HG induced miR-188-3p expression and the miR-188-3p antagonist abolished the HG-mediated increase in ROS. Notably, miR-188-3p was found to have a therapeutic effect against DN by aggravating mitochondrial damage and podocyte apoptosis. Germacrone alleviates DN progression in type I diabetes by limiting podocyte apoptosis, which was partly counteracted by miR-188-3p upregulation. The combination of germacrone and miR-188-3p antagonists is expected to be an effective therapeutic strategy for DN.
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