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. 2023 Aug 15;14:1164287. doi: 10.3389/fphys.2023.1164287

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Copyright © 2023 Liufu, Yu, Yu, Yu, Tian, Ou, Deng, Xing and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of the respiratory chain and the effects of NR and mitoLbNOX in m.3243A>G fibroblasts. (A) Complex I oxidizes NADH and regenerates NAD⁺, dysfunction of complex I leads to NADH accumulation and NAD⁺ depletion. (B) NR treatment and mitoLbNOX expression replenish m.3243A>G fibroblasts with NAD⁺, and mitoLbNOX exerts a greater effect by consuming the excess NADH accumulated in cells. MitoLbNOX, mitochondria-targeted H₂O-forming NADH oxidase; NAD, nicotinamide adenine dinucleotide; NADH, nicotinamide adenine dinucleotide + hydrogen; NR, nicotinamide riboside.