Autophagy in glomerular health and disease

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Autophagy in glomerular health and disease. / Hartleben, Björn; Wanner, Nicola; Huber, Tobias B.

In: SEMIN NEPHROL, Vol. 34, No. 1, 01.2014, p. 42-52.

Research output: SCORING: Contribution to journalSCORING: Review articleResearch

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@article{e03b114d02614f888b562c69b6d1b067,
title = "Autophagy in glomerular health and disease",
abstract = "Glomerular filtration coupled to tubular reabsorption was the prerequisite for one of the most important milestones in evolution, when animals made their way from water onto land. To fulfill the enormous filtration task the filter is composed of the most sophisticated postmitotic epithelial cells--the podocytes, which have only a very limited ability to regenerate. Podocyte injury and loss owing to genetic, toxic, immunologic, or metabolic insults underlie the most common glomerular diseases. Thus, the understanding of the factors and mechanisms that help to maintain podocytes are of major clinical importance. Recently, autophagy emerged as a key mechanism to eliminate unwanted cytoplasmic materials, thereby preventing cellular damage and stress to safeguard long-lived podocytes. Here, we highlight the accumulating evidence suggesting that autophagy plays a critical role in the homeostasis of podocytes during glomerular disease and aging.",
keywords = "Animals, Autophagy, Cell Aging, Cell Differentiation, Diabetic Nephropathies, Glomerulosclerosis, Focal Segmental, Homeostasis, Humans, Kidney Glomerulus, Lysosomal Storage Diseases, Podocytes, Journal Article, Research Support, Non-U.S. Gov't, Review",
author = "Bj{\"o}rn Hartleben and Nicola Wanner and Huber, {Tobias B}",
note = "{\textcopyright} 2014 Published by Elsevier Inc.",
year = "2014",
month = jan,
doi = "10.1016/j.semnephrol.2013.11.007",
language = "English",
volume = "34",
pages = "42--52",
journal = "SEMIN NEPHROL",
issn = "0270-9295",
publisher = "W B SAUNDERS CO-ELSEVIER INC",
number = "1",

}

RIS

TY - JOUR

T1 - Autophagy in glomerular health and disease

AU - Hartleben, Björn

AU - Wanner, Nicola

AU - Huber, Tobias B

N1 - © 2014 Published by Elsevier Inc.

PY - 2014/1

Y1 - 2014/1

N2 - Glomerular filtration coupled to tubular reabsorption was the prerequisite for one of the most important milestones in evolution, when animals made their way from water onto land. To fulfill the enormous filtration task the filter is composed of the most sophisticated postmitotic epithelial cells--the podocytes, which have only a very limited ability to regenerate. Podocyte injury and loss owing to genetic, toxic, immunologic, or metabolic insults underlie the most common glomerular diseases. Thus, the understanding of the factors and mechanisms that help to maintain podocytes are of major clinical importance. Recently, autophagy emerged as a key mechanism to eliminate unwanted cytoplasmic materials, thereby preventing cellular damage and stress to safeguard long-lived podocytes. Here, we highlight the accumulating evidence suggesting that autophagy plays a critical role in the homeostasis of podocytes during glomerular disease and aging.

AB - Glomerular filtration coupled to tubular reabsorption was the prerequisite for one of the most important milestones in evolution, when animals made their way from water onto land. To fulfill the enormous filtration task the filter is composed of the most sophisticated postmitotic epithelial cells--the podocytes, which have only a very limited ability to regenerate. Podocyte injury and loss owing to genetic, toxic, immunologic, or metabolic insults underlie the most common glomerular diseases. Thus, the understanding of the factors and mechanisms that help to maintain podocytes are of major clinical importance. Recently, autophagy emerged as a key mechanism to eliminate unwanted cytoplasmic materials, thereby preventing cellular damage and stress to safeguard long-lived podocytes. Here, we highlight the accumulating evidence suggesting that autophagy plays a critical role in the homeostasis of podocytes during glomerular disease and aging.

KW - Animals

KW - Autophagy

KW - Cell Aging

KW - Cell Differentiation

KW - Diabetic Nephropathies

KW - Glomerulosclerosis, Focal Segmental

KW - Homeostasis

KW - Humans

KW - Kidney Glomerulus

KW - Lysosomal Storage Diseases

KW - Podocytes

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

KW - Review

U2 - 10.1016/j.semnephrol.2013.11.007

DO - 10.1016/j.semnephrol.2013.11.007

M3 - SCORING: Review article

C2 - 24485029

VL - 34

SP - 42

EP - 52

JO - SEMIN NEPHROL

JF - SEMIN NEPHROL

SN - 0270-9295

IS - 1

ER -