Results 211 to 220 of about 4,864,586 (342)
Oral aspirin administration induces intestinal expansion of Lactobacillus murinus and Lactobacillus johnsonii, which suppresses the progression of atherosclerosis. This microbial expansion significantly enhances butyrate production by providing lactate as a metabolic substrate, thereby fostering the growth of butyrate‐producing bacteria. Butyrate plays
Rui Hua+15 more
wiley +1 more source
Musculoskeletal Tissue Banking
openaire +2 more sources
This study uncovers STAT6‐driven pulmonary fibrosis (PF) via suppression of PRKN‐mediated airway epithelial mitophagy, triggering mitochondrial dysfunction and ferroptosis. Rifabutin is identified as a potent STAT6 inhibitor that effectively reverses fibrotic progression. These findings reveal the STAT6‐PRKN axis as a pathogenic regulator and provide a
Youjing Yang+7 more
wiley +1 more source
Impact of Formalin- and Cryofixation on Raman Spectra of Human Tissues and Strategies for Tumor Bank Inclusion [PDF]
Giulia Mirizzi+11 more
openalex +1 more source
The DNA demethylase TET3 drives lipid metabolic reprogramming in pancreatic ductal adenocarcinoma via a non‐catalytic mechanism. TET3 recruits histone deacetylases to repress GATA6, sustaining lipogenic enzyme expression and ferroptosis resistance.
Shuai Liu+8 more
wiley +1 more source
This study highlights GRK2 is a central mediator in OSS‐induced endothelial dysfunction. OSS activates GPCRs in endothelial cells, leading to GRK2 phosphorylation and the activation of AP‐1. AP‐1 induces inflammation, while also promoting NR4A1 expression and anchoring LKB1 in the nucleus, which suppresses AMPK activity. This cascade causes endothelial
Li‐Da Wu+18 more
wiley +1 more source
Epidemiological data confirm obesity elevates thoracic aortic dissection (TAD) risk. Patient analyses implicate hyperleptinemia, where leptin binding to vascular smooth muscle cell (VSMC) receptors triggers Socs3‐mediated suppression of Stat5a transcriptional activity.
Ling Chen+18 more
wiley +1 more source
Activation of Kir4.1 Channels by 2‐D08 Promotes Myelin Repair in Multiple Sclerosis
Multiple sclerosis causes myelin loss and neurological dysfunction. This study shows that 2‐D08, a small molecule targeting Kir4.1 channels, promotes OPCs differentiation via FYN tyrosine kinase phosphorylation and the FYN/MYRF pathway. It significantly improves myelin repair and motor deficits in EAE mice and marmosets, highlighting its potential as a
Mingdong Liu+17 more
wiley +1 more source