Results 121 to 130 of about 102,753 (263)
Endothelial YAP Signaling Promotes Blood‐Spinal Cord Barrier Repair in Mice After Spinal Cord Injury
Endothelial YAP is required for blood‐spinal cord barrier repair after spinal cord injury. YAP‐dependent vascular repair is associated with ANGPT1/PI3K/AKT signaling in vivo and may involve endothelial‐pericyte paracrine interactions. By supporting vascular remodeling, tight junction restoration, restored pericyte coverage, and astrocyte‐vascular ...
Jiawei Wang +14 more
wiley +1 more source
Systematic Multi‐Level Analyses Decode the Arthritis‐Neurodegeneration Axis With In Vivo Validation
Arthritis and neurodegeneration are usually studied as separate disorders, but this study connects them through population evidence, genetic inference, transcriptomic mapping, and mouse models. It highlights RNF40 as a context‐dependent joint‐brain candidate, induced in inflammatory joints yet functionally linked to dopamine‐neuron vulnerability ...
Jinwen Wang +7 more
wiley +1 more source
Astrocyte‐specific SHP1 deletion disrupts astrocyte–vascular interactions and compromises BBB integrity while enhancing STAT1‐dependent CXCL10 expression. These changes synergistically promote peripheral CD4+ and CD8+ T‐cell infiltration into the SDH. The infiltrating T cells secrete IFN‐γ, which in turn activates microglia.
Lan‐Xing Yi +7 more
wiley +1 more source
FES‐derived MGE spheroids exhibit progenitor‐stage alterations in developmental trajectory and hypoxia‐responsive transcriptional programs, followed by functional disruption. Gestational hypoxia recapitulates impaired progenitor proliferation, shortened cell‐cycle progression, interneuron developmental abnormalities, and schizophrenia‐like behaviors in
Peiyan Ni +17 more
wiley +1 more source
PTEN knockdown activates AKT phosphorylation, promoting Nrf2 nuclear translocation and STAT3 activation, which upregulates GPX4 and antioxidant enzymes HO‐1, SOD1, SOD2, and NQO1. These coordinated changes reduce lipid peroxidation and ROS, inhibit ferroptosis, and ultimately ameliorate cognitive impairment in APP/PS1 transgenic mice, highlighting a ...
Da‐Wei Wang +5 more
wiley +1 more source
A Small‐Molecule DEPTAC Rescues Cognitive Deficits by Targeted Dephosphorylation of Pathological Tau
TP2 is a fully synthetic small‐molecule dephosphorylation‐targeting chimera that recruits endogenous PP2A‐Bα to Tau, enabling targeted removal of pathological phosphate modifications. In two tauopathy mouse models, systemic TP2 reduces Tau pathology, preserves neuronal and synaptic integrity, improves neuroimmune homeostasis, and rescues cognition ...
Fei Sun +12 more
wiley +1 more source
Endothelial miR‐15a/16‐1 deletion promotes long‐term recovery after traumatic brain injury by restoring SYNE1 expression. Enhanced endothelial SYNE1 preserves vascular integrity, protects white and gray matter, and improves neurological function. The endothelial miR‐15a/16‐1–SYNE1 axis emerges as a key regulator of neurovascular repair and a potential ...
Shun Li +17 more
wiley +1 more source
A multifunctional EV‐based nanoplatform (Ang‐TEVs@Gel) was engineered via preconditioning, surface targeting, and ROS‐responsive hydrogel encapsulation to reprogram microglia. This system restored autophagy via miR‐664a‐3p/PIK3CA axis, cleared myelin debris, resolved neuroinflammation, and promoted axon remyelination, ultimately achieving robust motor ...
Wu Xiong +17 more
wiley +1 more source
In microglia, STAT3 upregulates TAB2, which promotes NF‐κB activation through its NZF domain‐mediated recognition of K63‐linked ubiquitin chains, leading to inflammatory cytokine release and subsequent neuronal injury. Lumacaftor suppresses TAB2 expression and directly binds the TAB2‐NZF domain to interrupt K63 ubiquitin recognition, thereby blocking ...
Yanhao Zhao +12 more
wiley +1 more source

