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Tubulointerstitial nephritis antigen-like 1 promotes the progression of liver fibrosis after HCV eradication with direct-acting antivirals.
Int J Biol Sci
January 2025
CAMS Key Laboratory of Antiviral Drug Research, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
Although therapies based on direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus (HCV) in patients, there is still a high risk of liver fibrosis even after a sustained virological response. Therefore, it is of great clinical importance to understand the mechanism of potential factors that promote liver fibrosis after virological cure by treatment with DAAs. Here, we found that tubulointerstitial nephritis antigen-like 1 (TINAGL1) is significantly increased in HCV-infected hepatocytes and in the liver of patients with liver fibrosis, and that higher TINAGL1 expression persists in HCV-eradicated hepatocytes after treatment with DAAs.
View Article and Find Full Text PDFEndothelial-secreted Endocan activates PDGFRA and regulates vascularity and spatial phenotype in glioblastoma.
Nat Commun
January 2025
The Intellectual and Developmental Disabilities Research Center, The Semel Institute for Neuroscience and Human Behavior, and The Broad Stem Cell Research Center, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Extensive neovascularization is a hallmark of glioblastoma (GBM). In addition to supplying oxygen and nutrients, vascular endothelial cells provide trophic support to GBM cells via paracrine signaling. Here we report that Endocan (ESM1), an endothelial-secreted proteoglycan, confers enhanced proliferative, migratory, and angiogenic properties to GBM cells and regulates their spatial identity.
View Article and Find Full Text PDFAnandamide Inhibits Vascular Smooth Muscle Migration, Endothelial Adhesion Protein Expression and Monocyte Adhesion of Human Coronary Artery Cells.
Cells
December 2024
Institute of Pharmacology and Toxicology, Rostock University Medical Center, Schillingallee 70, 18057 Rostock, Germany.
Endocannabinoids have been shown to play a complex role in the pathophysiology of a number of cardiovascular disorders. In the present study, the effects of the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were investigated in human coronary artery smooth muscle cells (HCASMC) and human coronary artery endothelial cells (HCAEC) with regard to potential atheroprotective and anti-inflammatory effects. In HCASMC, AEA showed an inhibitory effect on platelet-derived growth factor-induced migration, but not proliferation, independent of major cannabinoid-activatable receptors (CB, CB, TRPV1), while 2-AG left both responses unaffected.
View Article and Find Full Text PDFModeling the Impact of Extracellular Vesicle Cargoes in the Diagnosis of Coronary Artery Disease.
Biomedicines
November 2024
Department of Genetics, Cell and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.
: We aimed to assess the relationship among circulating extracellular vesicles (EVs), hypoxia-related proteins, and the conventional risk factors of life-threatening coronary artery disease (CAD) to find more precise novel biomarkers. : Patients were categorized based on coronary CT angiography. Patients with a Segment Involvement Score > 5 were identified as CAD patients.
View Article and Find Full Text PDFHigh glucose couples DJ-1 with PTEN to activate PDGFRβ for renal proximal tubular cell injury.
PLoS One
January 2025
VA Research, Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas, United States of America.
Article Synopsis
- The study investigates how high glucose levels in diabetes lead to kidney cell damage through the activation of a signaling pathway involving DJ-1 and PTEN.
- DJ-1 is found to be upregulated in kidney cells under high glucose conditions, which triggers the Akt/mTORC1 signaling pathway, resulting in cell growth and fibrosis.
- The research indicates that inhibiting DJ-1 can prevent glucose-induced cell growth and damage, while overexpressing DJ-1 replicates the harmful effects, highlighting its role in renal injury related to diabetes.
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