CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury

Injuries in the embryonal kidney can be repaired by a cell migratory response but how this is regulated at a molecular level is unclear. Here, the authors show in mice that deletion of Cxcl12 and Myc delays pronephros injury repair by changing mitochondrial metabolism and glycolysis.

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Autores principales: Toma A. Yakulov, Abhijeet P. Todkar, Krasimir Slanchev, Johannes Wiegel, Alexandra Bona, Martin Groß, Alexander Scholz, Isabell Hess, Anne Wurditsch, Florian Grahammer, Tobias B. Huber, Virginie Lecaudey, Tillmann Bork, Jochen Hochrein, Melanie Boerries, Justine Leenders, Pascal de Tullio, François Jouret, Albrecht Kramer-Zucker, Gerd Walz
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/1c3d2a42e5234ad3afafeb44b9152fbb
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Sumario:Injuries in the embryonal kidney can be repaired by a cell migratory response but how this is regulated at a molecular level is unclear. Here, the authors show in mice that deletion of Cxcl12 and Myc delays pronephros injury repair by changing mitochondrial metabolism and glycolysis.