Effects and mechanisms of Polygonati Rhizoma polysaccharide on potassium oxonate and hypoxanthine-induced hyperuricemia in mice

International Journal of Biological Macromolecules, Год журнала: 2024, Номер unknown, С. 135550 - 135550

Опубликована: Сен. 1, 2024

Язык: Английский

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Protective Role of Vitamin D Receptor Against Mitochondrial Calcium Overload from PM2.5-Induced Injury in Renal Tubular Cells

Redox Biology, Год журнала: 2025, Номер unknown, С. 103518 - 103518

Опубликована: Янв. 1, 2025

Язык: Английский

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Mitochondrial dysfunction in acute kidney injury

Renal Failure, Год журнала: 2024, Номер 46(2)

Опубликована: Авг. 27, 2024

Acute kidney injury (AKI) is a systemic clinical syndrome increasing morbidity and mortality worldwide in recent years. Renal tubular epithelial cells (TECs) death caused by mitochondrial dysfunction one of the pathogeneses. The imbalance quality control main cause dysfunction. Mitochondrial plays crucial role AKI. mechanisms are involved regulating integrity function, including antioxidant defense, control, DNA (mtDNA) repair, dynamics, mitophagy, biogenesis. Currently, many studies have used as targeted therapeutic strategy for Therefore, this review aims to present latest research advancements on AKI, providing valuable reference theoretical foundation prevention treatment condition, ultimately enhancing patient prognosis.

Язык: Английский

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Single-cell transcriptomics in a child with coenzyme Q10 nephropathy: potential of single-cell RNA sequencing in pediatric kidney disease

Pediatric Nephrology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 14, 2025

Abstract Background Coenzyme Q10 (CoQ10) nephropathy is a well-known cause of hereditary steroid-resistant nephrotic syndrome, primarily impacting podocytes. This study aimed to elucidate variations in individual cell-level gene expression CoQ10 using single-cell transcriptomics. Methods We conducted sequencing kidney biopsy specimen from 5-year-old boy diagnosed with caused by compound heterozygous COQ2 mutation complicated immune complex-mediated glomerulonephritis. The analysis focused on the proportion cell types, differentially expressed genes each type, and changes related mitochondrial function oxidative phosphorylation (OXPHOS). Results Our findings revealed uniform downregulation across various types context these mutations. Notably, there was specific decrease all types. also highlighted an altered population attributed mutation. Pathway indicated OXPHOS upregulation synthesis pathways, particularly Conclusions improves our understanding nephropathy’s pathogenesis highlights potential applications pediatric diseases. Graphical

Язык: Английский

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Targeting Sting and Protecting Mitochondrial Function with Nephropathy Ⅱ Decoction to Alleviate Renal Fibrosis

Опубликована: Янв. 1, 2025

Язык: Английский

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Targeting oxidative stress-induced lipid peroxidation enhances podocyte function in cystinosis

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Фев. 20, 2025

Cystinosis is a rare, incurable lysosomal storage disease caused by mutations in the CTNS gene encoding cystine transporter cystinosin, which leads to accumulation all cells of body. Patients with cystinosis display signs podocyte damage characterized extensive loss podocytes into urine at early stages, glomerular proteinuria, and development focal segmental glomerulosclerosis (FSGS) lesions. Although standard treatment cysteamine decreases cellular levels, it neither reverses injury nor prevents podocytes. Thus, pathogenic mechanisms other than are involved dysfunction cystinosis. We used immortalized patient-derived cystinosis, healthy, knockdown investigate The results were validated our newly in-house developed fluorescent ctns-/-[Tg(fabp10a:gc-EGFP)] zebrafish larvae model. To understand impaired functionality, static dynamic permeability assays, tracer-metabolomic analysis, flow cytometry, western blot, chemical redox-sensing probes used. In current study, we discovered that demonstrate increased ferroptotic cell death mitochondrial reactive oxygen species (ROS)-driven membrane lipid peroxidation. Moreover, present fragmented network tricarboxylic acid cycle (TCA) energy metabolism. Targeting ROS peroxidation improved function vitro rescued proteinuria vivo larvae. Mitochondrial contribute driving ferroptosis, turn lead detachment. This finding adds list podocytopathies associated dysfunction. identified reveal new therapeutic targets highlight as an exploitable vulnerability

Язык: Английский

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Genipin attenuates oxidative damage in periodontal tissues by alleviating mitochondrial dysfunction and abnormal glucose uptake through inhibition of UCP2

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 26, 2025

Introduction Periodontitis is a chronic inflammatory disease closely associated with mitochondrial dysfunction. Uncoupling protein 2 (UCP2), located in the inner membrane of mitochondria, reduces potential (MMP) and adenosine triphosphate (ATP) synthesis by promoting proton leakage across membrane. This leads to decreased energy metabolism efficiency, impairing cellular glucose uptake, disrupting intracellular balance. Genipin (GP), recognized UCP2 inhibitor, exhibits anti-inflammatory antioxidant properties. study aimed investigate specific role GP periodontal tissue redox signaling mechanism development periodontitis. Methods In this study, we constructed model H O -induced oxidative stress human ligament cells (hPDLCs). vivo , rat periodontitis was established evaluate effects mechanisms alleviating damage tissues cells. Results Cell experiments showed that effectively alleviated dysfunction hPDLCs inhibiting expression function, restoring cell viability, reducing apoptosis. Additionally, intervention increased transporter 4 (GLUT4), thereby uptake. The results animal demonstrated reduced alveolar bone resorption destruction rats periodontitis, inhibited osteoclast differentiation, improved tissue, promoted GLUT4 expression, levels Discussion regulates maintaining homeostasis, enhancing playing central role.

Язык: Английский

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Spatially resolved multi-omics reveals the renal cortex-metabolic reprogramming of Shenhua Tablet for intervention on IgA nephropathy

Phytomedicine, Год журнала: 2025, Номер 141, С. 156742 - 156742

Опубликована: Апрель 14, 2025

Язык: Английский

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Targeting STING and protecting mitochondrial function with Nephropathy Ⅱ Decoction to alleviate renal fibrosis

Phytomedicine, Год журнала: 2025, Номер unknown, С. 156785 - 156785

Опубликована: Апрель 1, 2025

Язык: Английский

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Morphometric study of proximal tubular cell mitochondria using TEM images in renal diseases

Ultrastructural Pathology, Год журнала: 2025, Номер unknown, С. 1 - 11

Опубликована: Апрель 24, 2025

The kidney is rich in mitochondria, and any alterations or damage to tubular cell mitochondria play an important role renal metabolic activities the pathogenesis of various diseases. Quantitative analysis mitochondrial concentration, size, shape essential for understanding biology disorders. This study assessed morphometric parameters proximal convoluted adjacent glomerulus different disorders investigated how they correlated with serum creatinine. A total 65 biopsy cases received by transmission electron microscope (TEM) laboratory diagnosis were included study. TEM images glutaraldehyde-osmium tetroxide fixed epoxy-resin embedded 70 nm thick sections used evaluation (i) minor axis(MinX) (ii) major axis(MajX) (iii) Area, (iv)Perimeter, (v) Aspect ratio (vi) Roundness cells using QuPath software. Mitochondrial density (MDensity), % space (MSpace), surface (MSDensity) cytoplasm estimated each sample. Serum creatinine showed good negative correlations MSpace MSDensity, elongation was more disorder comparison normal histology, which indicated variation concentration could be features function disorder.

Язык: Английский

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