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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: Trends Cell Biol. 2014 Apr 29;24(8):464–471. doi: 10.1016/j.tcb.2014.04.002

Figure 4.

Figure 4

Electron transport via NADH generates NAD+ in mitochondria and may decline with age. In young mitochondria, NADH, made by the citric acid cycle, readily donates its electrons to complex I of the electron transport chain (ETC) and thereby generates NAD+. During the aging process, DNA damage accumulates in the nucleus, causing PARP activation and NAD+ reduction. Consequently, SIRT1 activity is reduced, resulting in increased PGC-1α acetylation and decreased TFAM levels. These nuclear events might reduce mitochondrial function in old mitochondria by affecting mitochondrial complex I and other mitochondrial components, or blocking the entry of electrons from NADH into the ETC, thereby creating an NAD deficiency.