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Effects of GH/IGF on the Aging Mitochondria
The mitochondria are key organelles regulating vital processes in the eukaryote cell. A decline in mitochondrial function is one of the hallmarks of aging. Growth hormone (GH) and the insulin-like growth factor-1 (IGF-1) are somatotropic hormones that regulate cellular homeostasis and play significa...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7349719/ https://www.ncbi.nlm.nih.gov/pubmed/32498386 http://dx.doi.org/10.3390/cells9061384 |
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author | Poudel, Sher Bahadur Dixit, Manisha Neginskaya, Maria Nagaraj, Karthik Pavlov, Evgeny Werner, Haim Yakar, Shoshana |
author_facet | Poudel, Sher Bahadur Dixit, Manisha Neginskaya, Maria Nagaraj, Karthik Pavlov, Evgeny Werner, Haim Yakar, Shoshana |
author_sort | Poudel, Sher Bahadur |
collection | PubMed |
description | The mitochondria are key organelles regulating vital processes in the eukaryote cell. A decline in mitochondrial function is one of the hallmarks of aging. Growth hormone (GH) and the insulin-like growth factor-1 (IGF-1) are somatotropic hormones that regulate cellular homeostasis and play significant roles in cell differentiation, function, and survival. In mammals, these hormones peak during puberty and decline gradually during adulthood and aging. Here, we review the evidence that GH and IGF-1 regulate mitochondrial mass and function and contribute to specific processes of cellular aging. Specifically, we discuss the contribution of GH and IGF-1 to mitochondrial biogenesis, respiration and ATP production, oxidative stress, senescence, and apoptosis. Particular emphasis was placed on how these pathways intersect during aging. |
format | Online Article Text |
id | pubmed-7349719 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-73497192020-07-15 Effects of GH/IGF on the Aging Mitochondria Poudel, Sher Bahadur Dixit, Manisha Neginskaya, Maria Nagaraj, Karthik Pavlov, Evgeny Werner, Haim Yakar, Shoshana Cells Review The mitochondria are key organelles regulating vital processes in the eukaryote cell. A decline in mitochondrial function is one of the hallmarks of aging. Growth hormone (GH) and the insulin-like growth factor-1 (IGF-1) are somatotropic hormones that regulate cellular homeostasis and play significant roles in cell differentiation, function, and survival. In mammals, these hormones peak during puberty and decline gradually during adulthood and aging. Here, we review the evidence that GH and IGF-1 regulate mitochondrial mass and function and contribute to specific processes of cellular aging. Specifically, we discuss the contribution of GH and IGF-1 to mitochondrial biogenesis, respiration and ATP production, oxidative stress, senescence, and apoptosis. Particular emphasis was placed on how these pathways intersect during aging. MDPI 2020-06-02 /pmc/articles/PMC7349719/ /pubmed/32498386 http://dx.doi.org/10.3390/cells9061384 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Poudel, Sher Bahadur Dixit, Manisha Neginskaya, Maria Nagaraj, Karthik Pavlov, Evgeny Werner, Haim Yakar, Shoshana Effects of GH/IGF on the Aging Mitochondria |
title | Effects of GH/IGF on the Aging Mitochondria |
title_full | Effects of GH/IGF on the Aging Mitochondria |
title_fullStr | Effects of GH/IGF on the Aging Mitochondria |
title_full_unstemmed | Effects of GH/IGF on the Aging Mitochondria |
title_short | Effects of GH/IGF on the Aging Mitochondria |
title_sort | effects of gh/igf on the aging mitochondria |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7349719/ https://www.ncbi.nlm.nih.gov/pubmed/32498386 http://dx.doi.org/10.3390/cells9061384 |
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