Results 141 to 150 of about 621,617 (245)

Matrix Rigidity Mechanoprimes Microglia for Inflammation Through Cytoskeletal‐to‐Nuclear Signaling and 3D Spatio‐Epigenomic Remodeling

open access: yesAdvanced Science, EarlyView.
Pathological tissue rigidity mechanoprimes microglia by enhancing actin cytoskeleton–nucleus coupling and chromatin opening at rigidity‐responsive cis‐regulatory elements (mechanoCREs). Subsequent NF‐κB/p65 signaling converges on this permissive regulatory state to amplify inflammatory gene expression and microglial activation.
Yu Xuan Meng   +15 more
wiley   +1 more source

Multi‐Tissue Crosstalk Regulating Meniscus Healing Under Inflammation and Physiological Loading

open access: yesAdvanced Science, EarlyView.
Using a novel Meniscus‐on‐a‐chip (MoC) model integrated with a meniscus‐specific bioreactor, this study investigated the roles of multi‐tissue crosstalk that regulates injury, healing, and degeneration of the meniscus injury under inflammation and pathophysiological loading.
Hun Jin Jeong   +5 more
wiley   +1 more source

An Extracellular Pore‑Targeting Peptide Defines a Designable Allosteric Site in TRPV2

open access: yesAdvanced Science, EarlyView.
Structure‐guided peptide engineering yields Depiv2, a highly potent and subtype‐selective TRPV2 inhibitor that binds to the extracellular pore and remodels it into a closed, non‐conductive state. Depiv2 suppresses pathological cardiac hypertrophy, establishing the TRPV2 outer pore as a designable interface for selective peptide modulation.
Aiqin Zhu   +7 more
wiley   +1 more source

Acid‐Responsive Nanobot‐Integrated Core‐Shell Microneedles Reprogram the Degenerative Annulus Fibrosus Microenvironment Through Epigenetic Suppression of Ferroptosis

open access: yesAdvanced Science, EarlyView.
An acid‐responsive core‐shell microneedle system normalizes the degenerative annulus fibrosus microenvironment by consuming pathological H+, generating O2, and providing NIR‐amplified redox buffering. Mechanistically, it epigenetically suppresses ferroptosis via DNMT3A‐dependent methylation of the ATF3 promoter, relieving ATF3‐mediated repression of ...
Lu Tan   +7 more
wiley   +1 more source

Persistent Zn2+ Influx‐Mediated Deacetylation of ANXA2 Regulates the “Zn2+‐Autophagic Flux” and Alleviates Intervertebral Disc Degeneration

open access: yesAdvanced Science, EarlyView.
Zinc transporter SLC39A14 sustains intracellular Zn2+ levels to activate SIRT3‑dependent ANXA2 deacetylation at K302. This modification weakens ANXA2‑mTOR binding and releases autophagic‑flux suppression in nucleus pulposus cells. Dysregulated Zn2+ homeostasis disrupts this axis to drive intervertebral disc degeneration.
Yuxin Jin   +23 more
wiley   +1 more source

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