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Celastrol ameliorates fibrosis in Western diet/tetrachloromethane-induced nonalcoholic steatohepatitis by suppressing Notch/osteopontin signaling.
Phytomedicine
January 2025
Department of Gastroenterology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China. Electronic address:
Background: Celastrol was recently identified as a potential treatment for obesity and hepatic steatosis. However, whether Celastrol effectively suppresses the nonalcoholic fatty liver disease (NAFLD) stage remains unknown. This study aimed to evaluate the role of Celastrol in the progression from simple steatosis to nonalcoholic steatohepatitis (NASH) and fibrosis.
View Article and Find Full Text PDFInfiltrative classical monocyte-derived and SPP1 lipid-associated macrophages mediate inflammation and fibrosis in ANCA-associated glomerulonephritis.
Nephrol Dial Transplant
December 2024
Amsterdam UMC location University of Amsterdam, Department of Internal Medicine, section of Nephrology, Amsterdam, The Netherlands.
Background And Hypothesis: Kidney macrophage infiltration is a histological hallmark of vasculitic lesions and is strongly linked to disease activity in anti-neutrophil cytoplasmic antibodies (ANCA)-associated glomerulonephritis (AGN). The precise mechanisms by which kidney macrophages influence local inflammation and long-term damage remain largely unknown.
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LINC01089 governs the miR-1287-5p/HSPA4 axis to negatively regulate osteogenic differentiation of mesenchymal stem cells.
Bone Joint Res
December 2024
Department of Orthopedics, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China.
Aims: The involvement of long non-coding RNA (lncRNA) in bone marrow mesenchymal stem cell (MSC) osteogenic differentiation during osteoporosis (OP) development has attracted much attention. In this study, we aimed to disclose how LINC01089 functions in human mesenchymal stem cell (hMSC) osteogenic differentiation, and to study the mechanism by which LINC01089 regulates MSC osteogenesis.
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Inhibition of SLC40A1 represses osteoblast formation via inducing iron accumulation and activating the PERK/ATF4/CHOP pathway mediated oxidative stress.
Redox Rep
December 2024
Department of Orthopedics, Medical Affairs Department, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, People's Republic of China.
Article Synopsis
- The study investigates how SLC40A1 affects iron levels, oxidative stress, and the differentiation of bone cells called osteoblasts.
- SLC40A1 was manipulated in mouse preosteoblastic cells to observe changes in these factors, revealing that inhibiting SLC40A1 led to increased iron and oxidative stress and decreased differentiation markers.
- The findings suggest that blocking SLC40A1 hampers osteoblast formation by promoting iron buildup and triggering a specific stress response pathway, indicating a potential target for influencing bone health.
HIF-1α knockdown attenuates phenotypic transformation and oxidative stress induced by high salt in human aortic vascular smooth muscle cells.
Sci Rep
November 2024
Department of Geriatrics, The First Affiliated Hospital of Dali University, Dali, 671000, Yunnan, China.
Increased dietary salt intake is a well-established risk factor for hypertension and related cardiovascular diseases, involving complex vascular remodeling processes. However, the specific role of hypoxia-inducible factor-1α (HIF-1α) in vascular pathophysiology under high-salt conditions remains poorly understood. This study investigates the role of HIF-1α in high-salt-induced vascular remodeling using human aortic vascular smooth muscle cells (HA-VSMCs) cultured in vitro.
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