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Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense

Aging is associated with increased inflammation and alterations in mitochondrial biogenesis, which promote the development of cardiovascular diseases. Emerging evidence suggests a role for sirtuins, which are NAD(+)-dependent deacetylases, in the regulation of cardiovascular inflammation and mitocho...

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Autores principales: Barcena de Arellano, Maria Luisa, Pozdniakova, Sofya, Kühl, Anja A., Baczko, Istvan, Ladilov, Yury, Regitz-Zagrosek, Vera
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6503880/
https://www.ncbi.nlm.nih.gov/pubmed/30964749
http://dx.doi.org/10.18632/aging.101881
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author Barcena de Arellano, Maria Luisa
Pozdniakova, Sofya
Kühl, Anja A.
Baczko, Istvan
Ladilov, Yury
Regitz-Zagrosek, Vera
author_facet Barcena de Arellano, Maria Luisa
Pozdniakova, Sofya
Kühl, Anja A.
Baczko, Istvan
Ladilov, Yury
Regitz-Zagrosek, Vera
author_sort Barcena de Arellano, Maria Luisa
collection PubMed
description Aging is associated with increased inflammation and alterations in mitochondrial biogenesis, which promote the development of cardiovascular diseases. Emerging evidence suggests a role for sirtuins, which are NAD(+)-dependent deacetylases, in the regulation of cardiovascular inflammation and mitochondrial biogenesis. Sirtuins are regulated by sex or sex hormones and are decreased during aging in animal models. We hypothesized that age-related alterations in cardiac Sirt1 and Sirt3 occur in the human heart and examined whether these changes are associated with a decrease in anti-oxidative defense, inflammatory state and mitochondrial biogenesis. Using human ventricular tissue from young (17-40 years old) and old (50-68 years old) individuals, we found significantly lower Sirt1 and Sirt3 expression in old female hearts than in young female hearts. Additionally, lower expression of the anti-oxidative protein SOD2 was observed in old female hearts than in young female hearts. Aging in female hearts was associated with a significant increase in the number of cardiac macrophages and pro-inflammatory cytokines, as well as NF-kB upregulation, indicating a pro-inflammatory shift. Aging-associated pathways in the male hearts were different, and no changes in Sirt1 and Sirt3 or cardiovascular inflammation were observed. In conclusion, the present study revealed a female sex-specific downregulation of Sirt1 and Sirt3 in aged hearts, as well as a decline in mitochondrial anti-oxidative defense and a pro-inflammatory shift in old female hearts but not in male hearts.
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spelling pubmed-65038802019-05-17 Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense Barcena de Arellano, Maria Luisa Pozdniakova, Sofya Kühl, Anja A. Baczko, Istvan Ladilov, Yury Regitz-Zagrosek, Vera Aging (Albany NY) Research Paper Aging is associated with increased inflammation and alterations in mitochondrial biogenesis, which promote the development of cardiovascular diseases. Emerging evidence suggests a role for sirtuins, which are NAD(+)-dependent deacetylases, in the regulation of cardiovascular inflammation and mitochondrial biogenesis. Sirtuins are regulated by sex or sex hormones and are decreased during aging in animal models. We hypothesized that age-related alterations in cardiac Sirt1 and Sirt3 occur in the human heart and examined whether these changes are associated with a decrease in anti-oxidative defense, inflammatory state and mitochondrial biogenesis. Using human ventricular tissue from young (17-40 years old) and old (50-68 years old) individuals, we found significantly lower Sirt1 and Sirt3 expression in old female hearts than in young female hearts. Additionally, lower expression of the anti-oxidative protein SOD2 was observed in old female hearts than in young female hearts. Aging in female hearts was associated with a significant increase in the number of cardiac macrophages and pro-inflammatory cytokines, as well as NF-kB upregulation, indicating a pro-inflammatory shift. Aging-associated pathways in the male hearts were different, and no changes in Sirt1 and Sirt3 or cardiovascular inflammation were observed. In conclusion, the present study revealed a female sex-specific downregulation of Sirt1 and Sirt3 in aged hearts, as well as a decline in mitochondrial anti-oxidative defense and a pro-inflammatory shift in old female hearts but not in male hearts. Impact Journals 2019-04-08 /pmc/articles/PMC6503880/ /pubmed/30964749 http://dx.doi.org/10.18632/aging.101881 Text en Copyright © 2019 Barcena de Arellano et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Barcena de Arellano, Maria Luisa
Pozdniakova, Sofya
Kühl, Anja A.
Baczko, Istvan
Ladilov, Yury
Regitz-Zagrosek, Vera
Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title_full Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title_fullStr Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title_full_unstemmed Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title_short Sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
title_sort sex differences in the aging human heart: decreased sirtuins, pro-inflammatory shift and reduced anti-oxidative defense
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6503880/
https://www.ncbi.nlm.nih.gov/pubmed/30964749
http://dx.doi.org/10.18632/aging.101881
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