Gospodaryov · Biochimica et biophysica acta. Bioenergetics 2025 · narrative review · n=?

Alternative NADH dehydrogenase: A complex I backup, a drug target, and a tool for mitochondrial gene therapy.

Cited 11 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review of preclinical and mechanistic studies with no primary human data.

PubMed 39615731 · doi:10.1016/j.bbabio.2024.149529 · record verified 2026-08-26

What was done

This narrative review synthesizes literature on alternative NADH dehydrogenase (type II NADH dehydrogenase, or NDH-2). It covers its molecular structure, resistance to rotenone, lack of proton-pumping activity, phylogenetic distribution across bacteria, fungi, plants, and certain animals, its role as an antimicrobial drug target, and its use in model organisms as a gene therapy tool to bypass mitochondrial complex I defects.

What was found

The abstract provides no numerical data or quantitative effect sizes. It reports that expressing NDH-2 in model organisms ameliorates complex I-related pathologies (including Parkinson's disease models) and extends lifespan. Proposed mechanisms for longevity extension include modulation of the NAD+/NADH ratio, reduction in mitochondrial reactive oxygen species (ROS) generation, or mitohormetic induction of defense pathways via transient ROS increases.

Why it matters

Because mammalian complex I is a massive, multi-subunit assembly prone to mutation and oxidative damage, the single-subunit NDH-2 provides a simplified functional bypass for mitochondrial respiratory deficiency and a potential target for gene therapy.

Limits

The paper is a qualitative review with no meta-analysis or original empirical data. All therapeutic and longevity findings are limited to non-human model organisms. Because NDH-2 does not pump protons, it restores redox balance but produces less ATP per NADH oxidized than native complex I, the long-term metabolic trade-offs of which remain unproven in humans.

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