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A New Pathogenesis of Albuminuria: Role of Transcytosis
Author(s) -
Fang-Fang He,
Yi Gong,
Zhenqiong Li,
Liang Wu,
Haiyue Jiang,
Hua Su,
Chun Zhang,
Yumei Wang
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000490223
Subject(s) - transcytosis , albuminuria , endocytosis , pathogenesis , reabsorption , renal physiology , microbiology and biotechnology , kidney , biology , medicine , endocrinology , receptor
Transcytosis is an important intracellular transport process by which multicellular organisms selectively move cargoes from apical to basolateral membranes without disrupting cellular homeostasis. In kidney, macromolecular components in the serum, such as albumin, low-density lipoprotein and immunoglobulins, pass through the glomerular filtration barrier (GFB) and proximal tubular cells (PTCs) by transcytosis. Protein transcytosis plays a vital role in the pathology of albuminuria, which causes progressive destruction of the GFB structure and function. However, the pathophysiological consequences of protein transcytosis in the kidney remain largely unknown. This article summarizes recent researches on the regulation of albumin transcytosis across the GFB and PTCs in both physiological and pathological conditions. Understanding the mechanism of albumin transcytosis may reveal potential therapeutic targets for prevention or alleviation of the pathological consequences of albuminuria.

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