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. 2024 Apr 3;20(1):41–53. doi: 10.4103/NRR.NRR-D-23-01921

Figure 1.

Figure 1

Schematic diagram depicting the metabolic processes that are potentially regulated by PQQ under physiological conditions and may provide neuroprotection.

PQQ has been reported to influence many metabolic mechanisms fueling tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS), thus regulating basic cell metabolism. In particular, PQQ can modulate cell metabolism by influencing amino acid and lipid metabolism, acting as lactate dehydrogenase (LDH) cofactor, promoting nicotinamide adenine dinucleotide (NAD) synthesis, inducing mitochondrial biogenesis and complexes expression. These mechanisms can be regulated by PQQ either singularly or synergistically, in a very context-dependent manner among different systems. The modulation of these metabolic processes can improve TCA cycle and potentiate the oxidative phosphorylation (OXPHOS), thus resulting in increased adenosine 5′-triphosphate (ATP) production. The neuroprotective properties of PQQ documented in many different models of neurodegeneration may be related to its capacity to promote neuronal metabolism, although in some contexts this strict association needs to be further confirmed (and hence indicated in the figure by the green dotted arrow). Created with Microsoft PowerPoint. PQQ: Pyrroloquinoline quinone.