Results 301 to 310 of about 1,216,905 (389)

Emodin Alleviates Sepsis‐Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL‐10

open access: yesAdvanced Science, EarlyView.
Emodin targets BCL‐10 to modulate the BCL‐10/MALT1 complex, thereby suppressing NF‐κB activation and significantly exerting multiorgan protective effects in sepsis. Abstract Sepsis is a life‐threatening condition caused by dysregulated host responses to infection, characterized by excessive inflammation and abnormal coagulation.
Xiaolong Xu   +16 more
wiley   +1 more source

NIR Driven Pd/Cerium Oxide Nano‐Heterojunction for Enhanced Salvaging Sepsis Induced Acute Liver Injury via Reprogramming Redox Homeostasis in Synergy with Inducing Autophagy

open access: yesAdvanced Science, EarlyView.
In vivo SALI therapy is achieved by scavenging intracellular ROS levels, downregulating inflammatory factors expression levels, inducing macrophage M2 directional polarization, and activating Keap1/Nrf‐2/HO‐1 pathway to reprogram redox homeostasis, induce cellular autophagy, reduce systemic inflammation, and promote liver tissue repair. Abstract Sepsis
Tao Qin   +21 more
wiley   +1 more source

Inhibition of UBE2C Promotes Parkin‐Mediated K63‐Linked Ubiquitination of TOP2A to Induce Senescence and Increase Sensitivity of Doxorubicin in Breast Cancer

open access: yesAdvanced Science, EarlyView.
In the study, UBE2C was found to be significantly overexpressed in breast cancer and transcriptionally regulated by FOXM1. Inhibition of UBE2C suppressed proliferation, induced senescence, and sensitized breast cancer cells to doxorubicin. Mechanistically, UBE2C inhibition promoted Parkin‐mediated K63‐linked ubiquitination of TOP2A.
Yihui Yang   +12 more
wiley   +1 more source

In Situ Proliferating Peptide Nanoparticle Augments Multi‐Target Intervention of Secondary Brain Damage Following Subarachnoid Hemorrhage

open access: yesAdvanced Science, EarlyView.
This work designs an in situ proliferating peptide nanoparticle as a flexible resolution that modulates the neuro‐glia unit to enable enhanced multi‐target combinational therapy for secondary brain damage following subarachnoid hemorrhage. Abstract Subarachnoid hemorrhage (SAH), a lethal stroke subtype, involves complex pathological cascades triggered ...
Yibin Zhang   +8 more
wiley   +1 more source

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