The PM2.5 component, benzo[b]fluoranthene, may contribute to the pathogenesis of membranous nephropathy by activating phosphoinositide 3-kinase/protein kinase B pathway and causing podocyte pyroptosis.

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Tác giả: Qi Feng, Duopin Li, Peipei Li, Chang Liu, Dongwei Liu, Zhangsuo Liu, Shaokang Pan, Yan Shi, Wenjie Sun, Fei Tian, Xianpeng Zhang, Yilin Zhang

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Netherlands : International immunopharmacology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 713605

 Membranous nephropathy (MN) is the main type of adult nephrotic syndrome, and its prevalence is increasing annually. An increasing number of studies have suggested that the pathogenesis of MN is related to 2.5-μm particulate matter (PM2.5), but the underlying mechanism has not been elucidated fully. Elucidating this mechanism can help prevent and treat MN. The constituents of PM2.5 vary from place to place
  hence, the component responsible for PM2.5-related MN is still unclear. This study investigated the effects of benzo[b]fluoranthene (BbF), a PM2.5 component, on pyroptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway in Sprague-Dawley rats and mouse podocytes. The organic constituents of BbF in PM2.5 can enter the circulatory system through the lungs and act on the kidneys to cause kidney damage, possibly because BbF activates the PI3K/AKT pathway and causes podocytes to undergo pyroptosis.
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