Literature DB >> 22388550

Mammalian target of rapamycin signaling in the podocyte.

Ken Inoki1, Tobias B Huber.   

Abstract

PURPOSE OF REVIEW: Mammalian target of rapamycin (mTOR) is an evolutionarily conserved protein kinase. mTOR forms two distinct functional multiprotein kinase complexes that mutually phosphorylate different substrates and regulate a wide array of essential cellular processes including translation, transcription and autophagy. mTOR is active in several types of cancer and plays a role in a variety of other serious human diseases, including diabetes, neurodegenerative disorders and polycystic kidney disease. However, until recently, only very little was known about the function of mTOR in glomerular homeostasis. RECENT
FINDINGS: Emerging studies highlight the important roles of the mTOR signaling pathway in both maintaining and deregulating glomerular and podocyte function.
SUMMARY: Here we review the current understanding of mTOR signaling in podocyte biology and discuss its implications for the development of glomerular diseases.

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Year:  2012        PMID: 22388550     DOI: 10.1097/MNH.0b013e3283520f38

Source DB:  PubMed          Journal:  Curr Opin Nephrol Hypertens        ISSN: 1062-4821            Impact factor:   2.894


  19 in total

1.  Amino Acids Regulate mTORC1 by an Obligate Two-step Mechanism.

Authors:  Julia Dyachok; Svetlana Earnest; Erica N Iturraran; Melanie H Cobb; Elliott M Ross
Journal:  J Biol Chem       Date:  2016-09-01       Impact factor: 5.157

Review 2.  Mechanisms and biological functions of autophagy in diseased and ageing kidneys.

Authors:  Sophie Fougeray; Nicolas Pallet
Journal:  Nat Rev Nephrol       Date:  2014-11-11       Impact factor: 28.314

3.  Autophagy modulates endoplasmic reticulum stress-induced cell death in podocytes: a protective role.

Authors:  Yu-Chi Cheng; Jer-Ming Chang; Chien-An Chen; Hung-Chun Chen
Journal:  Exp Biol Med (Maywood)       Date:  2014-10-15

4.  Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys.

Authors:  Bairbre A McNicholas; Diana G Eng; Julia Lichtnekert; Peter S Rabinowitz; Jeffrey W Pippin; Stuart J Shankland
Journal:  Am J Physiol Renal Physiol       Date:  2016-07-20

5.  Rheb/mTORC1 signaling promotes kidney fibroblast activation and fibrosis.

Authors:  Lei Jiang; Lingling Xu; Junhua Mao; Jianzhong Li; Li Fang; Yang Zhou; Wei Liu; Weichun He; Allan Zijian Zhao; Junwei Yang; Chunsun Dai
Journal:  J Am Soc Nephrol       Date:  2013-05-09       Impact factor: 10.121

6.  Targeting mTOR Signaling Can Prevent the Progression of FSGS.

Authors:  Stefan Zschiedrich; Tillmann Bork; Wei Liang; Nicola Wanner; Kristina Eulenbruch; Stefan Munder; Björn Hartleben; Oliver Kretz; Simon Gerber; Matias Simons; Amandine Viau; Martine Burtin; Changli Wei; Jochen Reiser; Nadja Herbach; Maria-Pia Rastaldi; Clemens D Cohen; Pierre-Louis Tharaux; Fabiola Terzi; Gerd Walz; Markus Gödel; Tobias B Huber
Journal:  J Am Soc Nephrol       Date:  2017-03-07       Impact factor: 10.121

7.  Sestrin 2: a regulator of the glomerular parietal epithelial cell phenotype.

Authors:  Bart Smeets; Tobias B Huber
Journal:  Am J Physiol Renal Physiol       Date:  2014-08-20

8.  The ability of remaining glomerular podocytes to adapt to the loss of their neighbours decreases with age.

Authors:  James van der Wolde; Kotaro Haruhara; Victor G Puelles; David Nikolic-Paterson; John F Bertram; Luise A Cullen-McEwen
Journal:  Cell Tissue Res       Date:  2022-03-15       Impact factor: 4.051

9.  Rapamycin upregulates autophagy by inhibiting the mTOR-ULK1 pathway, resulting in reduced podocyte injury.

Authors:  Lingling Wu; Zhe Feng; Shaoyuan Cui; Kai Hou; Li Tang; Jianhui Zhou; Guangyan Cai; Yuansheng Xie; Quan Hong; Bo Fu; Xiangmei Chen
Journal:  PLoS One       Date:  2013-05-08       Impact factor: 3.240

10.  Understanding the mechanisms of proteinuria: therapeutic implications.

Authors:  Jorge E Toblli; P Bevione; F Di Gennaro; L Madalena; G Cao; M Angerosa
Journal:  Int J Nephrol       Date:  2012-07-04
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