Cargando…
Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity
For reasons that remain unclear, endogenous synthesis and tissue levels of coenzyme Q10 (CoQ10) tend to decline with increasing age in at least some tissues. When CoQ10 levels are sufficiently low, this compromises the efficiency of the mitochondrial electron transport chain, such that production of...
Autores principales: | , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8928362/ https://www.ncbi.nlm.nih.gov/pubmed/35296520 http://dx.doi.org/10.1136/openhrt-2021-001927 |
_version_ | 1784670625204273152 |
---|---|
author | DiNicolantonio, James J McCarty, Mark F O'Keefe, James H |
author_facet | DiNicolantonio, James J McCarty, Mark F O'Keefe, James H |
author_sort | DiNicolantonio, James J |
collection | PubMed |
description | For reasons that remain unclear, endogenous synthesis and tissue levels of coenzyme Q10 (CoQ10) tend to decline with increasing age in at least some tissues. When CoQ10 levels are sufficiently low, this compromises the efficiency of the mitochondrial electron transport chain, such that production of superoxide by site 2 increases and the rate of adenosine triphosphate production declines. Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span. Reduction of the cytoplasmic and mitochondrial NAD(+)/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD(+). The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms. And CoQ10 deficiency has also been found to lower mRNA expression of Sirt1. An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease. Hence, correction of CoQ10 deficiency joins a growing list of measures that have potential for amplifying health protective Sirt1/Sirt3 activities. |
format | Online Article Text |
id | pubmed-8928362 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-89283622022-04-01 Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity DiNicolantonio, James J McCarty, Mark F O'Keefe, James H Open Heart Coronary Artery Disease For reasons that remain unclear, endogenous synthesis and tissue levels of coenzyme Q10 (CoQ10) tend to decline with increasing age in at least some tissues. When CoQ10 levels are sufficiently low, this compromises the efficiency of the mitochondrial electron transport chain, such that production of superoxide by site 2 increases and the rate of adenosine triphosphate production declines. Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span. Reduction of the cytoplasmic and mitochondrial NAD(+)/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD(+). The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms. And CoQ10 deficiency has also been found to lower mRNA expression of Sirt1. An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease. Hence, correction of CoQ10 deficiency joins a growing list of measures that have potential for amplifying health protective Sirt1/Sirt3 activities. BMJ Publishing Group 2022-03-16 /pmc/articles/PMC8928362/ /pubmed/35296520 http://dx.doi.org/10.1136/openhrt-2021-001927 Text en © Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) . |
spellingShingle | Coronary Artery Disease DiNicolantonio, James J McCarty, Mark F O'Keefe, James H Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title | Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title_full | Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title_fullStr | Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title_full_unstemmed | Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title_short | Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity |
title_sort | coenzyme q10 deficiency can be expected to compromise sirt1 activity |
topic | Coronary Artery Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8928362/ https://www.ncbi.nlm.nih.gov/pubmed/35296520 http://dx.doi.org/10.1136/openhrt-2021-001927 |
work_keys_str_mv | AT dinicolantoniojamesj coenzymeq10deficiencycanbeexpectedtocompromisesirt1activity AT mccartymarkf coenzymeq10deficiencycanbeexpectedtocompromisesirt1activity AT okeefejamesh coenzymeq10deficiencycanbeexpectedtocompromisesirt1activity |