Results 151 to 160 of about 53,904 (254)

CD4+ Tregs Drive Post‐Ischemic Sprouting Angiogenesis via Endothelial YY1/MAML1 Reactivation

open access: yesAdvanced Science, EarlyView.
ABSTRACT Microvascular complications of diabetes are chronic diseases of small vessels. We previously found that CD4+ regulatory T‐cells (Tregs) are markedly reduced in type 2 diabetes (T2D) after ischemic injury in both mice and humans, and that Treg deficiency in immunodeficient mice impairs vascular regeneration.
Hang Qu   +10 more
wiley   +1 more source

Tumor‐Derived LAMB3 Drives Immunosuppressive LRRC15+ Fibroblast Formation During Pancreatic Ductal Adenocarcinoma Development

open access: yesAdvanced Science, EarlyView.
A single‐cell atlas of pancreatic ductal adenocarcinoma development reveals progressive ductal‐fibroblast‐immune crosstalk. Tumor‐derived LAMB3 drives the formation of immunosuppressive LRRC15+ fibroblasts through the ITGB1/FAK/MAPK/FOSL2 signaling. Glycolytic reprogramming upregulates LAMB3 and correlates with LRRC15+ fibroblast enrichment.
Xuqing Shi   +23 more
wiley   +1 more source

Mitigating Cancer Therapy–Related Cognitive Impairment by Targeted Activation of Undruggable Phosphatase

open access: yesAdvanced Science, EarlyView.
An RVG‑engineered exosomal saRNA delivery system (RVG‑EVs‑saPtpro) effectively targets and activates hippocampal PTPRO, functioning as a “molecular brake” to alleviate cancer therapy‑related cognitive impairment (CTRCI) by enhancing neuronal survival, neurogenesis, and synaptic plasticity.
Zhimeng Yao   +18 more
wiley   +1 more source

TSPYL5 Promotes Triple‐Negative Breast Cancer Metastasis by Antagonizing USP10‐Mediated PTEN Stabilization to Unleash a ZEB1‐Dependent EMT Program

open access: yesAdvanced Science, EarlyView.
The hyperactivation of PI3K/AKT signaling in PTEN wild‐type triple‐negative breast cancer represents a clinical paradox. We delineate a novel post‐translational regulatory axis wherein the oncogene TSPYL5 competitively antagonizes the deubiquitinase USP10.
Jiaying Shi   +8 more
wiley   +1 more source

Mitochondrial Dysfunction Unravels the Potential Molecular Link Between Night Shift Work‐Related Circadian Disruption and Elevated Blood Pressure in Human and Mouse Models

open access: yesAdvanced Science, EarlyView.
This diagram illustrates that night shift work disrupts circadian clock genes (like CLOCK, BMAL1) in both humans and mice. This disruption leads to mitochondrial dysfunction (imbalanced fusion/fission proteins) and increased oxidative stress, which is identified as the primary mechanism ultimately causing elevated blood pressure.
Zhaoqiang Jiang   +16 more
wiley   +1 more source

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