Results 181 to 190 of about 516,739 (277)

RGS16 Aggravates Hepatic Ischemia‐Reperfusion Injury via Hepatocyte‐Intrinsic Apoptosis/Inflammation & Neutrophil Recruitment/NETosis

open access: yesAdvanced Science, EarlyView.
RGS16 competitively interferes with the YTHDF3–PAN3 complex to prevent CXCL1 mRNA decay during hepatic ischemia‐reperfusion injury. Stabilized CXCL1 strengthens hepatocyte injury, neutrophil recruitment, and NET‐associated inflammation, uncovering how stress‐induced RGS16 converts post‐transcriptional regulation into immune‐mediated liver damage ...
Xinglong Li   +16 more
wiley   +1 more source

AI Designed Conformation Locking Peptides Target STING to Restore Diabetic Wound Healing

open access: yesAdvanced Science, EarlyView.
A generative AI pipeline identifies SCP‐1, a conformation‐locking peptide that stabilizes inactive STING. Incorporated into a dual‐responsive hydrogel for localized, MMP‐9‐triggered release, SCP‐1 suppresses inflammation, promotes reparative macrophage polarization, and accelerates diabetic wound healing.
Xinyu Li   +8 more
wiley   +1 more source

Reorganization of Innate Immune Cell Lipid Profiles by Bioinspired Meroterpenoids to Limit Inflammation

open access: yesAdvanced Science, EarlyView.
Resolution pharmacology is an emerging strategy to tackle inflammatory pathologies. Bioinspired meroterpenoids induce a lipid mediator class switch toward inflammation resolution in vitro and in vivo by targeting key nodes in lipid mediator biosynthesis and neutral lipid dynamics.
Lorenz Waltl   +20 more
wiley   +1 more source

B Cells are Activated via a Nanoporous Interface that Stabilizes Microvilli and Engages Mechanosensitive Ion Channels

open access: yesAdvanced Science, EarlyView.
B cells can be activated independently of antigen recognition via mechanical stimulation through nanoporous substrates. Exposure to such substrates induced B cell microvilli extension into the pores, intracellular Ca2+ signaling, phosphorylation of signaling proteins, and CD69 expression.
Nozie D. Aghaizu   +4 more
wiley   +1 more source

Crosstalk Between CTSB+ Glioblastoma Cells and S100A10+ Macrophages: A Self‐Reinforcing Circuit Promotes Immune Evasion and Limits Response to Immunotherapy

open access: yesAdvanced Science, EarlyView.
In glioblastoma, M2‐polarized macrophages secrete IL‐6, which activates STAT3 signaling in tumor cells to upregulate CTSB. Tumor‐derived CTSB binds the C‐terminus of macrophage S100A10, reinforcing M2 polarization and further IL‐6 secretion, thereby establishing a feedforward IL‐6/STAT3/CTSB/S100A10 loop. This cascade drives tumor growth, invasion, and
Hao Zhang   +11 more
wiley   +1 more source

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