Morphometric Effects of HO-1 Deficiency and Overexpression in Rat Glomeruli and Podocytes
Morphometric Effects of HO-1 Deficiency and Overexpression in Rat Glomeruli and Podocytes
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HO-1 缺乏和过度表达对大鼠肾小球和足细胞的形态学影响
DOI：
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发表时间：
2021
期刊：
影响因子：
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通讯作者：
E. Lianos
中科院分区：
文献类型：
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作者：
Kelsey Wilson;M. Detsika;E. Poulaki;H. Gakiopoulou;E. Lianos
在构成肾小球的各种细胞（内皮细胞、系膜细胞、常驻巨噬细胞和脏肾小球上皮细胞，也称为足细胞）中，后者最容易受到各种形式的肾小球损伤（糖尿病、高血压、免疫介导等），这些损伤经常进展为终末期肾病（ESKD）。这是由于它们的非复制性、终末分化的高度专门化性质。具体来说，它们表现出高的囊泡交通速率，这可以从它们的基底外侧区域的多个包被囊泡和包被坑中得到证明，并且由于发育良好的内质网和大的高尔基体[1]，它们具有高的蛋白质合成和翻译后修饰能力。损伤导致的足细胞耗竭是肾小球瘢痕形成（硬化）的一个公认机制，而进行性肾小球硬化导致ESKD[2]。因此，评估保护足细胞免受损伤的方法的策略正在被探索，这并不奇怪。
Of the various cells comprising the glomerulus (endothelial, mesangial, resident macrophages, and visceral glomerular epithelial cells also known as podocytes), the latter are most vulnerable to various forms of glomerular injury (Diabetes, Hypertension, immunemediated, etc.) that frequently progress to end-stage kidney disease (ESKD). This is due to their non-replicative, terminally differentiated highly specialized nature. Specifically, they exhibit a high rate of vesicular traffic as evidenced by multiple coated vesicles and coated pits along their basolateral domain and have a high capacity for protein synthesis and posttranslational modifications because of a well-developed endoplasmic reticulum and a large Golgi apparatus [1]. Podocyte depletion consequent to injury is a well-established mechanism underlying glomerular scarring (sclerosis) while progressive glomerulosclerosis leads to ESKD [2]. It is, therefore, not surprising that strategies assessing ways to protect podocytes against injury are being explored.
影响因子：
13.6
作者：
Binz-Lotter, Julia;Juengst, Christian;Hackl, Matthias J.
通讯作者：
Hackl, Matthias J.
影响因子：
13.6
作者：
Sato, Yuji;Wharram, Bryan L.;Wiggins, Roger C.
通讯作者：
Wiggins, Roger C.
影响因子：
13.6
作者：
Tan, Roderick J.;Zhou, Dong;Liu, Youhua
通讯作者：
Liu, Youhua