Results 201 to 210 of about 163,890 (298)

Engineered Peptide Self‐Assembled Nanofibers for Enhanced STING Activation: A Promising Nanodelivery Platform for Immunotherapy of Pediatric Solid Tumors

open access: yesAdvanced Science, EarlyView.
An engineered peptide self‐assembled nanofiber platform, designed to replicate STING–cGAMP binding motifs, facilitates pH‐responsive cytosolic delivery of cGAMP, enhances the endoplasmic reticulum with high efficiency, and robustly activates the STING pathway.
Yubin He   +6 more
wiley   +1 more source

AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

open access: yesAdvanced Science, EarlyView.
AI‐enabled de novo design of a TREM1 binder, integrated into a BBB‐crossing and macrophage‐targeted nanoplatform, enables TREM1 degradation and attenuates neuroinflammation, thereby promoting neuroprotection and tissue repair after traumatic brain injury. ABSTRACT Secondary neuroinflammation drives progressive damage after traumatic brain injury (TBI),
Yimin Huang   +19 more
wiley   +1 more source

Versatile Microgel Platform for Intervertebral Disc Degeneration Therapy: Targeting Pericyte‐Mediated Fibrosis and Protecting Nucleus Pulposus Cells

open access: yesAdvanced Science, EarlyView.
The engineered MMS@TRP microgel enables targeted, acid‐responsive delivery of a miR‐21 inhibitor to pericytes. It effectively suppresses disc fibrosis by inhibiting TGF‐β signaling while protecting nucleus pulposus cells via sustained, antioxidant tannic acid release.
Fei Ma   +12 more
wiley   +1 more source

Neonatal Sevoflurane Exposure Induces Long‐Term Cognitive Impairment via Epigenetically Mediated MMP9 Activation and Perineuronal Net Disruption in the Hippocampal CA2

open access: yesAdvanced Science, EarlyView.
Hippocampal CA2 perineuronal nets ensheathing excitatory pyramidal neurons are selectively vulnerable to repeated neonatal sevoflurane exposure. Epigenetic upregulation of MMP9 via reduced H3K27me3 disrupts PNN integrity, impairs BDNF–TrkB signaling, and causes synaptic protein loss and dendritic spine deficits, leading to persistent social and spatial
Lirong Liang   +11 more
wiley   +1 more source

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