Results 221 to 230 of about 186,093 (261)
PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury
Platelet activating factor (PAF) secreted by cardiomyocytes during MI/R, drives NETs formation and subsequent NETosis. PAF/NETosis signaling activation is an initiative and causal factor in driving MI/R injury. This study identifies dapagliflozin as a potent NETosis inhibitor, and demonstrates that manipulating PAF‐NETosis signal by dapagliflozin or ...
Jiawei Wu +11 more
wiley +1 more source
Corrigendum to A Case Report of Diabetic Ketoacidosis With Combined Use of a Sodium Glucose Transporter 2 Inhibitor and Hybrid Closed-Loop Insulin Delivery. [PDF]
europepmc +1 more source
This study investigates the impact of various post‐processing methods (filtration, sonication, dialysis, and heating) on lipid nanoparticles produced using microfluidics. The nanoparticles are designed for efficient delivery of miRNA into cells. The work highlights how processing conditions influence nanoparticle stability and quality, providing ...
Alicja Kosik‐Kozioł +8 more
wiley +1 more source
Protective Effects of Selective Mineralocorticoid Receptor Antagonist in Alport Syndrome on Top of Renin-Angiotensin-System/ Sodium-Glucose Transporter 2 Blockade. [PDF]
Song ZR, Li Y, Zhang H, Zhou XJ.
europepmc +1 more source
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
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
The engineered TF‐Fe@LC nanoplatform programs paraptotic death via multipath ROS amplification that disrupts redox homeostasis, provoking mitochondrial dysfunction, autophagic blockade, and ER stress. This caspase‐independent process elicits robust immunogenic cell death, combining with αPD‐L1 to activate systemic CD8+ T‐cell immunity and suppress ...
Zhe Yu +9 more
wiley +1 more source
This study tests NeuroD1 AAV‐based gene therapy in a non‐human primate Alzheimer's disease model. The therapy prevents neuronal damage, inhibits hippocampal atrophy, and reduces neuroinflammation. It also repairs vascular and blood‐brain barrier damage, restores cerebrospinal fluid biomarkers, enhances hippocampal glucose metabolism, and improves ...
Zhouquan Jiang +21 more
wiley +1 more source
Paraventricular CRF neurons in the hypothalamus project to glutamatergic neurons of the spinal trigeminal caudal nucleus, enhancing neuronal activation and CRFR2 signaling. This pathway increases CRF release and excitatory drive, promoting central sensitization and migraine‐related behaviors. Targeting the PVN–SP5C circuit provides a potential strategy
Jiang Bian +13 more
wiley +1 more source

