Abstract
Mitochondrial dysfunction within the tubular epithelium has been implicated in the pathogenesis of acute kidney injury. Inflammatory, ischemic, or toxic insults dysregulate mitochondrial dynamics, resulting in mitochondrial swelling, fission, and apoptosis. The coordinated processes of generating healthy mitochondria and clearing damaged organelles may contribute to the preservation and restoration of mitochondrial homeostasis. Emerging literature suggests that a master regulator of mitochondrial biogenesis, peroxisome proliferator-activated receptor-γ-coactivator-1α (PGC-1α), is highly expressed in the tubular epithelium of the healthy kidney, and its induction during the post-injury period may contribute to functional recovery from acute kidney injury.
Original language | English (US) |
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Pages (from-to) | 42-45 |
Number of pages | 4 |
Journal | Nephron - Clinical Practice |
Volume | 127 |
Issue number | 1-4 |
DOIs | |
State | Published - Apr 16 2014 |
Externally published | Yes |
Keywords
- Acute kidney injury
- Biogenesis
- Mitochondrial function
- Mitophagy
- Renal recovery
ASJC Scopus subject areas
- Nephrology