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TLR4

Isthmin 1 Is Expressed by Progenitor-Like Cells in the Lung: Phenotypical Analysis of Isthmin 1+ Hematopoietic Stem-Like Cells in Homeostasis and during Infection

[Journal of Immunology Research] Using multiparametric flow cytometry, scientists identified mesenchymal, endothelial, and hematopoietic progenitor cells that express the secreted small protein Isthmin 1.

Lipidomic Profiling of Bronchoalveolar Lavage Fluid Extracellular Vesicles Indicates Their Involvement in Lipopolysaccharide-Induced Acute Lung Injury

[Journal of innate Immunity] Extracellular vesicles released during acute lung injury originated from alveolar epithelial cells, macrophages, and neutrophils and carry a diverse array of lipid mediators derived from ω-3 and ω-6 polyunsaturated fatty acids.

Bench to Bedside — New Insights into the Pathogenesis of Necrotizing Enterocolitis

[Nature Reviews Gastroenterology & Hepatology] The authors provide new evidence explaining the pathogenesis of necrotizing enterocolitis (NEC), explore new findings indicating that NEC development has origins before birth, and discuss future questions and opportunities for discovery in this field.

Adiponectin Receptor Agonist Ameliorates Cardiac Lipotoxicity via Enhancing Ceramide Metabolism in Type 2 Diabetic Mice

[Cell Death & Disease] Phenotypic and metabolic profiles with associated cellular signaling pathways involved in lipid metabolism were investigated in the mice heart and human cardiomyocytes to establish treatment effect of adiponectin's agonists.

Hyperglycemia-Triggered ATF6-CHOP Pathway Aggravates Acute Inflammatory Liver Injury by β-Catenin Signaling

[Cell Death Discovery] Scientists demonstrated that in the liver tissues and Kupffer cells of diabetes mellitus patients and streptozotocin-induced hyperglycemic mice, the endoplasmic reticulum stress-ATF6-CHOP signaling pathway was activated.

Povidone Iodine Suppresses LPS-Induced Inflammation by Inhibiting TLR4/MyD88 Formation in Airway Epithelial Cells

[Scientific Reports] The authors explored the anti-inflammatory effects and underlying molecular mechanism of povidone-iodine (PVP-I) on lipopolysaccharide-stimulated airway epithelial cells and investigated whether nasal instillation of PVP-I could suppress mucosal inflammation in non-eosinophilic chronic rhinosinusitis mice.

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