Results 261 to 270 of about 619,300 (360)

TRIM56 Aggravates Cerebral Ischemia‐Reperfusion Injury via Inhibiting KLF4‐Activated Ferroptosis Signaling

open access: yesAdvanced Science, EarlyView.
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang   +15 more
wiley   +1 more source

Wearable and Implantable Devices for Continuous Monitoring of Muscle Physiological Activity: A Review

open access: yesAdvanced Science, EarlyView.
Recent advances in materials and device engineering enable continuous, real‐time monitoring of muscle activity via wearable and implantable systems. This review critically summarizes emerging technologies for tracking electrophysiological, biomechanical, and oxygenation signals, outlines fundamental principles, and highlights key challenges and ...
Zhengwei Liao   +4 more
wiley   +1 more source

A cell-specific computational framework reveals a pan-cancer hypoxia signature predicting overall survival and ICI response. [PDF]

open access: yesJ Biol Chem
Zhang C   +13 more
europepmc   +1 more source

Human Atlas of Tooth Decay Progression: Identification of Cellular Mechanisms Driving the Switch from Dental Pulp Repair Toward Irreversible Pulpitis

open access: yesAdvanced Science, EarlyView.
Tooth decay progression transforms the dental pulp response from repair to fibrosis. At early stages, stromal cells reprogram to repair the extra cellular matrix (ECM), blood vessels, and nerves, remodel and grow, keeping repair possible. In advanced decay, hypoxia, and vessel regression, in complement with an immune switch, fuel nerve degeneration and
Hoang Thai Ha   +12 more
wiley   +1 more source

HRS Degradation‐Induced Nicotinamide Deficiency in Placental Extracellular Vesicles Triggers Preeclampsia by Disrupting Maternal‐Fetal Immune Homeostasis

open access: yesAdvanced Science, EarlyView.
This study shows that lower NAM levels in PE‐derived pEVs correlate with disease severity. NAM‐deficient pEVs reduce Th1 and Th17 inhibition, leading to PE‐like symptoms. NAM in pEVs inhibits Th1 via SIRT1 and Th17 via macrophages. Reduced NAM in PE‐EVs is due to decreased HRS expression in trophoblasts, resulting from elevated HSP27.
Haiyi Fei   +10 more
wiley   +1 more source

Mechanisms for Hypoxia Detection in O2-Sensitive Cells

open access: bronze, 2004
Naoji Fujishiro   +3 more
openalex   +2 more sources

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