Results 201 to 210 of about 13,982 (300)

Targeting the GPX4–FUNDC1 Interaction with Magnesium Lithospermate B Attenuates Sepsis‐Associated Lung Injury

open access: yesAdvanced Science, EarlyView.
The diagram depicts the endothelial‐protective mechanism of magnesium lithospermate B (MLB) in sepsis‐associated lung injury. MLB binds GPX4 at Gly79, disrupts its interaction with FUNDC1, prevents mitophagy‐mediated GPX4 degradation, restores mitophagic flux, reduces ROS, and limits ferroptosis.
Zhixi Li   +10 more
wiley   +1 more source

ETV4 Promotes Colorectal Cancer Progression by Reprogramming Asparagine Metabolism to Remodel the Stromal Microenvironment

open access: yesAdvanced Science, EarlyView.
ETV4 coordinates a dual transcriptional program by upregulating MET and asparagine synthetase (ASNS). The resulting asparagine (Asn) secretion acts as a metabolic signal, reprogramming hepatic stellate cells (HSCs) and primary cancer‐associated fibroblasts (CAFs) toward an inflammatory phenotype. These activated stromal cells release HGF to sustain the
Dujiang Fu   +14 more
wiley   +1 more source

Blockchain-based secure MEC model for VANETs using hybrid networks. [PDF]

open access: yesSci Rep
Goud GV   +5 more
europepmc   +1 more source

A Soft Robotic Model for Simulating Heart Valve Disease and Cardiac Interventions

open access: yesAdvanced Science, EarlyView.
This paper introduces a fully synthetic fabrication methodology for a soft robotic, in‐vitro model of the left‐heart, complete with a functioning mitral valve apparatus. With a view towards patient‐specific modeling, we demonstrate physiological flow and pressure waveforms, tunable mitral valve function with clinical imaging compatibility, and its use ...
James Davies   +14 more
wiley   +1 more source

Promotion of DFU Wound Healing via BRG1–COL16A1 Axis in Fibroblasts

open access: yesAdvanced Science, EarlyView.
In normal wound healing, transcription factor BRG1 is upregulated and binds the COL16A1 promoter to enhance its expression, promoting fibroblast proliferation, migration, contraction, extracellular matrix deposition, and granulation tissue formation, thus accelerating wound closure.
Penghui Wang   +10 more
wiley   +1 more source

Calcium Channel Blockers Inhibit Pancreatic Neuroendocrine Neoplasms Progression via Cav1.2‐Epigenetic Circuit

open access: yesAdvanced Science, EarlyView.
Our study reveals a novel mechanism of a positive regulatory circuit between Cav1.2 and H3K27ac for pancreatic neuroendocrine neoplasms (pNENs) progression. Cav1.2 is identified as a crucial target for promoting disease progression and correlates with malignant behaviors, which are remarkably inhibited by the administration of calcium channel blockers (
Yangyinhui Yu   +12 more
wiley   +1 more source

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