Results 231 to 240 of about 279,791 (361)

CD3ɛ Nanobody‐Engineered Extracellular Vesicles Driving In Vivo Generation of TCE‐secreting CAR‐Ts for Solid Tumor Therapy With Memory Response and Minimal Immunogenicity

open access: yesAdvanced Science, EarlyView.
HEK‐293T‐derived CD3ε Nb‐engineered EVs to generate dual‐targeting CAR‐T cells directly in vivo. These EVs selectively deliver CAR.BiTE transgenes into T cells and reprogramed to HLA‐G/PD‐L1‐targeting effector cells with enhanced memory and persistence.
Shi‐Wei Huang   +27 more
wiley   +1 more source

Diabetes Mellitus Facilitates Gallstone Formation Through CXCR2‐NETs–Mediated Liver‐Bile Barrier Damage

open access: yesAdvanced Science, EarlyView.
Diabetes is an independent risk factor for gallstones. It upregulates CXCR2 expression in hepatic neutrophils, stimulating the formation of NETs that disrupt hepatocellular tight junctions and the liver‐bile barrier. NETs enter bile to accelerate gallstone development, while sarcosine inhibits CXCR2 and NETs production, effectively reducing diabetes ...
Chao Shi   +10 more
wiley   +1 more source

Selenoprotein H Functions as a PPARα Coactivator to Link Selenium Homeostasis to Hepatic Lipid Metabolism and Protect against Steatohepatitis

open access: yesAdvanced Science, EarlyView.
Our study identifies selenium deficiency as a hallmark of MASH pathogenesis. Dietary selenium supplementation enhances hepatic fatty acid oxidation (FAO) and attenuates MASH progression by activating the PPARα pathway via selenoprotein H (SELENOH). This selenium‐SELENOH‐PPARα nexus redefines the functional scope of selenoproteins, moving from redox ...
Yuwei Zhang   +11 more
wiley   +1 more source

ACSL1‐Dependent Microglial Lipoimmunometabolic Reprogramming Underlies Cognitive Deficits in Alcohol Use Disorder

open access: yesAdvanced Science, EarlyView.
This study reveals that chronic alcohol exposure selectively upregulates ACSL1 expression in prefrontal cortical microglia, driving lipid metabolism reprogramming and lipid droplet accumulation, which activates the NLRP3 inflammasome and sustains neuroinflammation. To reverse this process, a dual‐targeted lipid nanoparticle, siACSL1@LNP‐MR, is designed
Liang Hao   +8 more
wiley   +1 more source

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