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Cystatin C is associated with osteoporosis and fractures: An observational study based on Mendelian randomization analysis.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2024
Research for Genetic Epidemiology and Genomics, School of Public Health, Suzhou Medical College of Soochow University, Suzhou Jiangsu 215123, China.
Objectives: Osteoporosis is characterized by decreased bone mass and damaged bone microstructure, often leading to fragility fractures. Low bone mineral density is a key risk factor for fractures. Serum cystatin C (CysC), an endogenous marker of glomerular filtration rate, is negatively correlated with bone mineral density and may be a potential risk factor for osteoporosis.
View Article and Find Full Text PDFUBE2C Mediates Follicular Thyroid Carcinoma Invasion and Metastasis via K29-Specific Vimentin Ubiquitination.
Cancer Lett
March 2025
Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, 510080, China; Department of Thyroid and Hernia Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510080, China. Electronic address:
Follicular thyroid carcinoma (FTC) poses significant clinical challenges due to its vascular invasion tendency and distant metastasis potential, leading to poorer patient outcomes compared to other thyroid carcinomas. Although ubiquitin-conjugating enzyme E2C (UBE2C) has been widely studied in various cancers, its specific role in FTC progression remains insufficiently explored. This study demonstrates UBE2C's dual functionality in FTC through clinical analysis and experimental validation.
View Article and Find Full Text PDFEffects of PARP1 inhibitor PJ-34 on TGFα, IL-6, and IL-1β levels in diabetic nephropathy.
J Immunol
February 2025
Orthopedics Department, Central Hospital of Ezhou, Ezhou, China.
Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β.
View Article and Find Full Text PDFSCN3B is an Anti-breast Cancer Molecule with Migration Inhibition Effect.
Biochem Genet
March 2025
Department of Gynecology, People's Hospital of Jianshi, Enshi Tujia and Miao Autonomous Prefecture, Enshi City, Hubei Province, China.
Breast cancer is a prevalent and highly heterogeneous malignancy that continues to be a major global health concern. Voltage-gated sodium channels are primarily known for their role in neuronal excitability, but emerging evidence suggests their involvement in the pathogenesis of various cancers, including breast cancer. However, the effect of β-subunits on breast cancer cells is not yet studied.
View Article and Find Full Text PDFPKM2 knockout facilitates the activation of the AMPK/KLF4/ACADVL pathway, leading to increased oxidative degradation of fatty acids in TNBC.
Med Oncol
March 2025
School of Basic Medicine, Gannan Medical University, Ganzhou, 341000, Jiangxi, China.
This study unveils PKM2 as a master metabolic coordinator in triple-negative breast cancer (TNBC), governing the glycolysis-lipolysis balance through the AMPK/KLF4/ACADVL axis. We demonstrate stage-specific PKM2 upregulation in TNBC, with CRISPR/Cas9 knockout inducing dual metabolic reprogramming-suppressed glycolysis and activated lipid catabolism. Mechanistically, PKM2 ablation triggers AMPK-dependent nuclear translocation of KLF4, which directly activates ACADVL (mitochondrial β-oxidation rate-limiting enzyme), explaining lipid droplet depletion.
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