Purpose: Oxidative stress is a key contributor to the development of dysregulated inflammation in acute lung injury (ALI). A naturally occurring single nucleotide polymorphism in the key extracellular

NIAID Data Ecosystem40

Catechin regulates miR-182/GGPPS1 signaling pathway and inhibits LPS-induced acute lung injury in mice

肺损伤机制

药物信号通路

Acute lung injury (ALI) and resultant acute respiratory distress syndrome (ARDS) are detrimental inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective t

Taylor & Francis Group2024-02-16 更新30

Inhibition of M1 polarization in alveolar macrophages by vasoactive intestinal peptide attenuates LPS-induced acute lung injury in vivo and vitro

肺损伤机制

细胞极化调控

Vasoactive intestinal peptide (VIP) is one of the neurotransmitters released by nonadrenergic noncholinergic inhibitory nerve endings. In lung tissues, VIP can inhibit alveolar macrophage phagocytosis

NIAID Data Ecosystem60

Bulk RNA-seq analysis in pulmonary endothelial cells between saline and LPS group, WT (Fgfr1loxp/loxp) and endothelial Fgfr1-conditional knock out mice (Fgfr1i?EC/i?EC mice).

肺损伤机制

内皮细胞转录组

Endothelial cells (ECs) serve as a semipermeable barrier and play a key role in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). It is well known that fibroblast growth factor recep

NIAID Data Ecosystem30

Myeloid ROS remodels pulmonary microenvironment to protect lungs from acute lung injury

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