| First Author | Svensson K | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 7 | Pages | e0158716 |
| PubMed ID | 27463191 | Mgi Jnum | J:249286 |
| Mgi Id | MGI:6094510 | Doi | 10.1371/journal.pone.0158716 |
| Citation | Svensson K, et al. (2016) Loss of Renal Tubular PGC-1alpha Exacerbates Diet-Induced Renal Steatosis and Age-Related Urinary Sodium Excretion in Mice. PLoS One 11(7):e0158716 |
| abstractText | The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1alpha is a transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1alpha in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1alpha seems largely dispensable for basal renal physiology. However, the role of PGC-1alpha in renal mitochondrial biogenesis indicates that activation of PGC-1alpha in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction. |
