Suppressed mitochondrial biogenesis in folic acid-induced acute kidney injury and early fibrosis
LJ Stallons, RM Whitaker, RG Schnellmann - Toxicology letters, 2014 - Elsevier
Acute kidney injury (AKI) is a disease with mitochondrial dysfunction and a newly
established risk factor for the development of chronic kidney disease (CKD) and fibrosis. We
examined mitochondrial homeostasis in the folic acid (FA)-induced AKI model that develops
early fibrosis over a rapid time course. Mice given a single dose of FA had elevated serum
creatinine (3-fold) and urine glucose (2.2-fold) 1 and 2 d after injection that resolved by 4 d.
In contrast, peroxisome proliferator gamma coactivator 1α (PGC-1α) and mitochondrial …
established risk factor for the development of chronic kidney disease (CKD) and fibrosis. We
examined mitochondrial homeostasis in the folic acid (FA)-induced AKI model that develops
early fibrosis over a rapid time course. Mice given a single dose of FA had elevated serum
creatinine (3-fold) and urine glucose (2.2-fold) 1 and 2 d after injection that resolved by 4 d.
In contrast, peroxisome proliferator gamma coactivator 1α (PGC-1α) and mitochondrial …