| First Author | Yuan Q | Year | 2021 |
| Journal | Cell Death Dis | Volume | 12 |
| Issue | 8 | Pages | 792 |
| PubMed ID | 34392303 | Mgi Jnum | J:310844 |
| Mgi Id | MGI:6762213 | Doi | 10.1038/s41419-021-04085-w |
| Citation | Yuan Q, et al. (2021) CPT1alpha maintains phenotype of tubules via mitochondrial respiration during kidney injury and repair. Cell Death Dis 12(8):792 |
| abstractText | Impaired energy metabolism in proximal tubular epithelial cells (PTECs) is strongly associated with various kidney diseases. Here, we characterized proximal tubular phenotype alternations during kidney injury and repair in a mouse model of folic acid nephropathy, in parallel, identified carnitine palmitoyltransferase 1alpha (CPT1alpha) as an energy stress response accompanied by renal tubular dedifferentiation. Genetic ablation of Cpt1alpha aggravated the tubular injury and interstitial fibrosis and hampered kidney repair indicate that CPT1alpha is vital for the preservation and recovery of tubular phenotype. Our data showed that the lipid accumulation and mitochondrial mass reduction induced by folic acid were persistent and became progressively more severe in PTECs without CPT1alpha. Interference of CPT1alpha reduced capacities of mitochondrial respiration and ATP production in PTECs, and further sensitized cells to folic acid-induced phenotypic changes. On the contrary, overexpression of CPT1alpha protected mitochondrial respiration and prevented against folic acid-induced tubular cell damage. These findings link CPT1alpha to intrinsic mechanisms regulating the mitochondrial respiration and phenotype of kidney tubules that may contribute to renal pathology during injury and repair. |
