Mitohormesis is an adaptive response induced by a mild mitochondrial stress that promotes longevity
and metabolic health in different organisms. This mechanism has been proposed as the cause of the
increase in the survival in Coq7+/− (Mclk1+/−) mice, which show hepatic reduction of COQ7, early
mitochondrial dysfunction and increased oxidative stress. Our study shows that the lack of COQ9 in
Coq9Q95X mice triggers the reduction of COQ7, COQ6 and COQ5, which results in an increase in life
expectancy. However, our results reveal that the hepatic CoQ levels are not decreased and, therefore,
neither mitochondrial dysfunction or increased oxidative stress are observed in liver of Coq9Q95X mice.
These data point out the tissue specific differences in CoQ biosynthesis. Moreover, our results suggest
that the effect of reduced levels of COQ7 on the increased survival in Coq9Q95X mice may be due to
mitochondrial mechanisms in non-liver tissues or to other unknown mechanisms.This work was supported by grants from Ministerio de
Economía Competitividad, Spain, and the ERDF (Grant Number SAF2015-65786-R), from the Consejería de
Economía, Innovación, Ciencia y Empleo, Junta de Andalucía (grant number P10-CTS-6133) and from the
University of Granada (grant reference “UNETE”, UCE-PP2017-06). AHG is a “FPU fellow” from the Ministerio
de Educación Cultura y Deporte, Spain. MLS was a predoctoral fellow from the Consejería de Economía,
Innovación, Ciencia y Empleo, Junta de Andalucía. LCL was supported by the “Ramón y Cajal” National
Programme, Ministerio de Economía y Competitividad, Spain (RYC-2011-07643)
