Results 81 to 90 of about 109,193 (265)

Fatty Acid Binding Protein 5 Mediates Astrocytic Pyroptosis and Neuroinflammation in Epilepsy via cGAS/STING Pathway

open access: yesAdvanced Science, EarlyView.
Astrocytic FABP5 promotes mitochondrial stress, cGAS‐STING pathway activation, pyroptosis, and neuroinflammation in epilepsy, contributing to seizure pathology. Genetic targeting of FABP5 or pharmacological inhibition of STING alleviates epileptic phenotypes, highlighting a potential therapeutic strategy for epilepsy.
Chen Chen   +10 more
wiley   +1 more source

The Inflammasome in Reproductive Biology: A Promising Target for Novel Therapies

open access: yesFrontiers in Endocrinology, 2020
The inflammasome is a key regulator of innate immunity involved in the inflammatory response to infections as well as disease through the activation of caspase-1 and the processing of the inflammatory cytokines interleukin (IL)-1β and IL-18.
Juan Pablo de Rivero Vaccari   +2 more
doaj   +1 more source

A Pancreatitis‐Inspired Trypsinogen Nanoplatform Reprograms Tumor‐Associated Macrophages via NF‐κB for Pancreatic Cancer Immunotherapy

open access: yesAdvanced Science, EarlyView.
Trypsinogen‐loaded nanoparticles reprogram TAMs via NF‐κB/NLRP3, driving M2→M1 conversion and potent phagocytosis to unleash antitumor immunity. ABSTRACT Although reprogramming tumor‐associated macrophages (TAMs) represents a promising therapeutic strategy, approaches that are both precise and safe remain scarce.
Lei Cao   +7 more
wiley   +1 more source

Porcine Deltacoronavirus M Protein Binds NLRP3 to Promote Inflammasome Assembly via Competition with TRIM31

open access: yesAdvanced Science, EarlyView.
Porcine deltacoronavirus (PDCoV) infection induces severe intestinal inflammation and acute diarrhea in piglets, yet the molecular mechanism remains incompletely understood. The M protein activates NLRP3 inflammasome through dual mechanisms: direct binding to the NLRP3 LRR domain and disruption of TRIM31‐mediated K48‐linked ubiquitination.
Jinhui Hou   +11 more
wiley   +1 more source

Targeted Degradation of STING by a Neutrophil Membrane‐Coated Nanoplatform Suppresses Microglial Pyroptosis After Subarachnoid Hemorrhage

open access: yesAdvanced Science, EarlyView.
MG1@NM‐Px serves as a microglia‐targeted STING‐degrading nanoplatform for subarachnoid hemorrhage. Following systemic administration, it crosses the blood–brain barrier and accumulates in activated microglia. STP1‐mediated STING ubiquitination and degradation suppress MAPK/inflammasome signaling, GSDME‐mediated pyroptosis, and IL‐1β release, revealing ...
Ruotian Zhang   +13 more
wiley   +1 more source

Inflammasomes, neutrophil extracellular traps, and cholesterol

open access: yesJournal of Lipid Research, 2019
Activation of macrophage inflammasomes leads to interleukin (IL)-1β and IL-18 secretion and promotes atherosclerosis and its complications in mice and humans.
Alan R. Tall, Marit Westerterp
doaj   +1 more source

Membrane‐Active Peptide Protects Against Inflammation by Targeting NLRP3 Activation at the Trans‐Golgi Network

open access: yesAdvanced Science, EarlyView.
The membrane‐active peptide Pep19‐2.5 reduces harmful inflammation by blocking activation of the NLRP3 inflammasome at trans‐Golgi network membranes. By targeting key membrane interactions, Pep19‐2.5 suppresses inflammatory IL‐1β production and alleviates allergic airway inflammation in mice, leading to reduced immune cell infiltration and improved ...
Jonas Engelhardt   +16 more
wiley   +1 more source

Hollow Cu2O Nanozymes Enhance Probiotic Therapy for Colitis via Redox Homeostasis and TXNIP/NLRP3 Inflammasome Inhibition

open access: yesAdvanced Science, EarlyView.
Hollow cuprous oxide (H‐Cu2O) nanozymes feature enlarged catalytic surfaces for superior reactive oxygen species (ROS) scavenging. By efficiently neutralizing mucosal ROS, H‐Cu2O directly suppresses the TXNIP/NLRP3 inflammasome axis and restores intestinal epithelial barrier integrity.
Guangzhao Wang   +7 more
wiley   +1 more source

The inflammasome [PDF]

open access: yesCurrent Biology, 2005
Petrilli, Virginie   +2 more
openaire   +2 more sources

QRICH1 Disrupts Endoplasmic Reticulum Homeostasis and Amplifies NF‐κB Signaling in Periodontal Ligament Stem Cells to Exacerbate Diabetic Periodontitis

open access: yesAdvanced Science, EarlyView.
QRICH1 has been established as a key factor contributing to impaired osteogenic potential and accelerated apoptosis of PDLSCs in diabetic periodontitis. QRICH1 not only significantly enhances UPR‐associated apoptotic signaling but also amplifies NF‐κB‐mediated inflammatory responses. Its inhibition restores osteogenic capacity and reduces alveolar bone
Han Li   +9 more
wiley   +1 more source

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