| 書(shū)目名稱(chēng) | Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome | | 編輯 | Kazunari Kaneko | | 視頻video | http://file.papertrans.cn/639/638343/638343.mp4 | | 概述 | Brings together all of the latest research by top researchers on molecular mechanisms in the pathogenesis of INS.Represents one putative pathogenetic molecule in each chapter and reviews its role, mec | | 圖書(shū)封面 |  | | 描述 | .This comprehensive book reviews our current state of knowledge about the pathogenesis of idiopathic nephrotic syndrome (INS), which comprises a heterogeneous group of diseases with distinct histological characteristics, such as minimal-change nephrotic syndrome (MCNS), focal segmental glomerulosclerosis (FSGS), and idiopathic membranous nephropathy (IMN). As the word “idiopathic” indicates, the pathogenesis of INS remains unclear. Historically, T-cell dysfunction has been thought to play an important part in the pathogenesis of MCNS, while circulating vascular permeabilities have been believed to induce proteinuria in FSGS. The book further describes recent advances in molecular biology, which have allowed us to speculate on the interactions between visceral glomerular epithelial cells (podocytes) and the relative significance of several molecules in the pathogenesis of INS, such as reactive oxygen species, nuclear factor-kappa B, CD80, angiopoietin-like 4, cardiotrophin-like cytokine-1, and M-type phospholipase A2 receptor. The normally rapid pace of scientific progress occasionally devolves into a state of chaos, and the pathogenetic research on INS is one such case. This volume | | 出版日期 | Book 2016 | | 關(guān)鍵詞 | CD80; angiopoietin-like 4; focal segmental glomerulosclerosis (FSGS); idiopathic membranous nephropathy | | 版次 | 1 | | doi | https://doi.org/10.1007/978-4-431-55270-3 | | isbn_softcover | 978-4-431-56279-5 | | isbn_ebook | 978-4-431-55270-3 | | copyright | Springer Japan 2016 |
The information of publication is updating
|
|
|Archiver|手機(jī)版|小黑屋|
派博傳思國(guó)際
( 京公網(wǎng)安備110108008328)
GMT+8, 2025-10-14 10:32
發(fā)表于 2025-3-21 16:20:12
