Results 171 to 180 of about 90,445 (239)

Ultrasound Controlled‐Release Hydrogel Promotes Diabetic Wound Healing via Neuroimmune Modulation and Synergistic ROS Scavenging

open access: yesAdvanced Science, EarlyView.
This study presents an ultrasound‐responsive hydrogel (MCF@CA) that co‐delivers a neuropeptide (CGRP) and a ROS‐scavenging manganese porphyrin to diabetic wounds. The system restores neuro‐immune communication, reprograms macrophages toward an anti‐inflammatory phenotype, and clears excess ROS, thereby accelerating wound closure and promoting mature ...
Mofan Li   +9 more
wiley   +1 more source

Mitochondrial CircRNA CircMT‐RNR2 Safeguards Antioxidant Defense to Support Fibroblast Functions in Wound Repair

open access: yesAdvanced Science, EarlyView.
CircMT‐RNR2 promotes wound healing by enhancing fibroblast proliferation, migration, contraction, and extracellular matrix (ECM) production. It sustains mitochondrial redox balance by stabilizing the antioxidant protein PRDX3, thereby reducing ROS‐induced damage. In diabetic foot ulcers, hypoxia, hyperglycemia, and reduced FGF2 and EGF expression lower
Guanglin Niu   +13 more
wiley   +1 more source

Identification of A p300–SP1–BRD4 Transcriptional Axis as a Key Driver of AR Hyperactivation in Polycystic Ovarian Syndrome

open access: yesAdvanced Science, EarlyView.
This study reveals a pivotal epigenetic regulatory role for the histone acetyltransferase p300, demonstrating that its acetylation of histone 3 at lysine 18 and 27 (H3K18ac and H3K27ac), alongside the formation of the p300/BRD4/SP1 complex, drives AR activation and ovarian fibrosis in PCOS.
Zhengquan Zhu   +11 more
wiley   +1 more source

Chaperone‐Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction

open access: yesAdvanced Science, EarlyView.
This study demonstrates that inflammatory stimuli induce the acetylation‐triggered, chaperone‐mediated autophagic degradation of ubiquitin‐specific peptidase 9 X‐linked (USP9X) in macrophages. USP9X acts as a macrophage “inflammation switch” after myocardial infarction (MI). USP9X loss destabilizes tumor necrosis factor receptor‐associated factor (TRAF)
Biqing Wang   +7 more
wiley   +1 more source

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