| Popis: |
With one of the highest mitochondrial densities in the body, the kidneys consume approximately 10% of total oxygen while constituting only 0.5% of body mass. Renal respiration is linearly correlated to solute extraction, linking mitochondrial oxidative metabolism directly to tubular function. This fundamental role of mitochondria in renal health may become an “Achilles heel” under duress. Acute kidney injury (AKI) related to each major class of stressor—inflammation, ischemia, and toxins—exhibits early and prominent injury to mitochondria. The classic mitochondrial biogenesis regulator, PGC1α (PPARγ-coactivator-1α) may confer protection to the tubules against these stressors. Recent work proposes that renal PGC1α directly increases levels of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for energy metabolism that has recently also been proposed as an anti-aging factor. This mini-article presents a short summary of research on the topics of AKI, PGC1α, and NAD+ to focus on recent studies that propose a direct mechanism between the regulation of metabolic health and the ability to resist renal stressors. |
