Results 201 to 210 of about 105,169 (258)

Phocaeicola coprophilus‐Derived 6‐Methyluracil Attenuates Radiation‐Induced Intestinal Fibrosis by Suppressing the IDO1‐Kynurenine‐AHR Axis

open access: yesAdvanced Science, EarlyView.
IR‐induced dysbiosis depletes P. coprophilus and its metabolite 6‐methyluracil, leading to disinhibition of the IDO1‐Kyn‐AHR axis. This results in sustained fibroblast activation and collagen deposition, driving radiation induced intestinal fibrosis. ABSTRACT Therapeutic options for radiation‐induced intestinal fibrosis (RIF) remain limited. This study
Jiaxin Zhang   +11 more
wiley   +1 more source

Nature‐Inspired Surface Modification Strategy Reverses the Autophagic Flux Impairment of Mitochondrial Transplantation for Attenuating Ischemic Strokes

open access: yesAdvanced Science, EarlyView.
The functionalized starch modifies the mitochondrial surface and encapsulates resveratrol into the cavity of helices, facilitating a novel mitochondrial transplantation platform (MLSR). Upon internalization in recipient cells, MLSR triggers mitophagy and maintains positive autophagic flux through RIP1/RIP3 pathway inhibition.
Nisha Wang   +12 more
wiley   +1 more source

Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction

open access: yesAdvanced Science, EarlyView.
Progressive stiffening of the hepatic extracellular matrix and free fatty acid overload activate the mechanosensor Piezo1 in steatotic hepatocytes, inducing calcium influx and nuclear translocation of Yes‐associated protein. YAP‐dependent nuclear signaling further drives inflammatory and fibrotic gene programs, lipid metabolic reprogramming, and ...
Juan Ma   +15 more
wiley   +1 more source

PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
Platelet activating factor (PAF) secreted by cardiomyocytes during MI/R, drives NETs formation and subsequent NETosis. PAF/NETosis signaling activation is an initiative and causal factor in driving MI/R injury. This study identifies dapagliflozin as a potent NETosis inhibitor, and demonstrates that manipulating PAF‐NETosis signal by dapagliflozin or ...
Jiawei Wu   +11 more
wiley   +1 more source

Platelet-activating factor antagonists

Clinical Reviews in Allergy, 1995
The great number of PAF antagonists reviewed in this article clearly shows the tremendous effort made in the last 20 yr to explore the complex biological background of the mechanism of action of PAF and the potential clinical benefit of its antagonists. It is obvious that now highly potent, long-acting, and perorally applicable PAF-receptor antagonists
M, Koltai, P G, Braquet
openaire   +4 more sources

Platelet-Activating Factor

2007
Platelet-activating factor (PAF) is a potent mediator that occurs at very low concentrations in cells and tissues. Accurate quantitation of PAF has always been difficult because of the physicochemical properties of PAF and its structural similarity to several much more abundant phospholipids.
John S, Owen   +2 more
openaire   +3 more sources

Platelet-activating factor receptor

Prostaglandins & Other Lipid Mediators, 2002
Platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a biologically active phospholipid mediator. Although PAF was named for its potential to induce platelet aggregation, intense investigations have elucidated potent biological actions of PAF in a broad range of cell types and tissues.
Zen-ichiro, Honda   +2 more
openaire   +3 more sources

Platelet-Activating Factor Antagonists

Annual Review of Pharmacology and Toxicology, 1987
Over the past decade platelet-activating factor has achieved the status of an important inflammatory mediator. The scientific enthusiasm and number of research investigators, publications, and meetings recently devoted to PAF suggest that this mediator will be the subject of continued study in the foreseeable future.
R N, Saunders, D A, Handley
openaire   +2 more sources

Home - About - Disclaimer - Privacy