Results 171 to 180 of about 237,133 (291)

Endothelial Cell‐Specific Molecule‐1 (ESM1): An Endogenous Anticoagulant and Protective Factor in Venous Thrombosis

open access: yesAdvanced Science, EarlyView.
This study identifies ESM1 as an endogenous anticoagulant that modulates venous thrombosis. It shows that ESM1 deficiency triggers vascular occlusion in zebrafish and mice, whereas its restoration or overexpression prolongs clot‐formation time. Mechanistic analyses reveal that ESM1 activates HCII through its dermatan‐sulfate chain, uncovering a ...
Changsheng Chen   +10 more
wiley   +1 more source

Context-Dependent Roles of ANGPTL2-Mediated Inflammaging in Tissue Homeostasis, Pathological Tissue Remodeling, and Longevity. [PDF]

open access: yesAging Cell
Yumoto S   +8 more
europepmc   +1 more source

Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

open access: yesAdvanced Science, EarlyView.
The study demonstrated that connexin43 (Cx43) knockout caused arrhythmic phenotype and decreased proline content in vitro and in vivo. Mechanistically, Cx43 interacts with the amino acid transporter SNAT2 (sodium‐dependent neutral amino acid transporter), and its deficiency disrupts proline transport and metabolism.
Hangying Ying   +8 more
wiley   +1 more source

Macrophage TRIM21 Inhibition Ameliorates Murine Acute Pancreatitis via PHB2‐Mediated Mitochondrial Stabilization

open access: yesAdvanced Science, EarlyView.
Macrophage‐derived TRIM21 drives the progression of AP via ubiquitin‐proteasome‐mediated degradation of PHB2, leading to impaired PHB2‐mediated mitophagy. Therefore, accumulation of cytosolic mtDNA hyperactivates the cGAS‐STING signaling axis, thereby amplifying inflammatory cascades.
Yansong Xu   +7 more
wiley   +1 more source

Senescent Synovial Intimal Fibroblasts Aggravate Osteoarthritis by Regulating Macrophage Polarization and Chondrocyte Phenotype Through ANGPTL4‐α5β1 Axis

open access: yesAdvanced Science, EarlyView.
Senescent synovial intimal fibroblasts (SIF) are identified as key drivers of osteoarthritis. They promote M1 macrophage polarization and cartilage degeneration via the ANGPTL4–α5β1 axis, regulated by transcription factors EGR1 and ATF3. Pharmacological inhibition of this pathway alleviates disease, revealing SIF senescence as a promising therapeutic ...
Muhai Deng   +7 more
wiley   +1 more source

SIRT5–RAC2 Axis Drives Monocyte‐to‐Macrophage Differentiation to Promote Inflammatory Injury in Premature Ovarian Insufficiency

open access: yesAdvanced Science, EarlyView.
SIRT5 desuccinylates and stabilizes RAC2, activating CSF1R‐dependent signaling to drive monocyte differentiation into M0 macrophages and their polarization toward pro‐inflammatory M1 phenotypes in CTX‐induced premature ovarian insufficiency. Inhibiting the SIRT5‐RAC2 axis attenuates inflammation, reduces granulosa cell apoptosis, and preserves ...
Wenjing TanTai   +15 more
wiley   +1 more source

Deformable Eutectic Alloy With Near‐Theoretical Yield Strength via Hierarchical Nanoscale Multiphases and Sessile Defects

open access: yesAdvanced Science, EarlyView.
A CoCrFeNiTa0.4 eutectic high‐entropy alloy achieves a near‐theoretical yield strength of 2.6 GPa with 13.6% plasticity. This breakthrough stems from a hierarchical nanostructure (FCC‐Laves lamellae with L12/D022 precipitates), which alleviates the inter‐phase modulus/hardness mismatch through synergistic strengthening and toughening, guiding the ...
Yusha Luo   +10 more
wiley   +1 more source

Pro‐ATO/Allicin Liposomes for Dual‐Pathway Targeting of p53‐Mutant Tumors

open access: yesAdvanced Science, EarlyView.
Schematic illustration of the “pro‐ATO”/allicin liposomal strategy. Liposomal encapsulation improves the stability and bioavailability of both agents while masking allicin's odor. Upon release in the tumor microenvironment, ATO reactivates structural p53 mutants, and allicin inhibits ATR signaling while releasing H2S, collectively inducing synthetic ...
Xiaoling Xu   +11 more
wiley   +1 more source

Trojan Horse Strategy: How Biomimetic Nanomedicine Remodels the Tumor Microenvironment

open access: yesAdvanced Science, EarlyView.
This review focuses on biomimetic nanomedicines for tumor microenvironment (TME) remodeling, covering their diverse biomimetic types, design principles, and mechanisms of immune cell reprogramming and reversal of immunosuppressive microenvironments, with particular emphasis on their application in synergistic immunotherapy.
Wanrong Wang   +7 more
wiley   +1 more source

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