mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress

Medientyp: E-Artikel
Titel: mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress
Beteiligte: Grahammer, Florian; Haenisch, Nora; Steinhardt, Frederic; Sandner, Lukas; Roerden, Malte; Arnold, Frederic; Cordts, Tomke; Wanner, Nicola; Reichardt, Wilfried; Kerjaschki, Dontscho; Ruegg, Markus A.; Hall, Michael N.; Moulin, Pierre; Busch, Hauke; Boerries, Melanie; Walz, Gerd; Artunc, Ferruh; Huber, Tobias B.
Erschienen: Proceedings of the National Academy of Sciences, 2014
Erschienen in: Proceedings of the National Academy of Sciences
Sprache: Englisch
DOI: 10.1073/pnas.1402352111
ISSN: 0027-8424; 1091-6490
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Beschreibung: <jats:title>Significance</jats:title> <jats:p>Mammalian target of rapamycin complex 1 (mTORC1) inhibitors are commonly used as immunosuppressants in solid-organ transplantation and as antiproliferative agents in various cancers. Despite indications of serious renal adverse events caused by mTORC1 inhibition, the role of mTORC1 for renal epithelial function and homeostasis has remained elusive. Unexpectedly, tubular mTORC1 controls energy-driven urine-concentrating mechanisms by maintaining mitochondrial biogenesis. Under pathophysiological conditions, mTORC1-dependent mitochondrial biogenesis is essential for energy supply and adaptation in response to ischemia. These findings identify mTORC1 as an important regulator of tubular energy metabolism, transcellular transport processes, and ischemic stress responses.</jats:p>
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