TGF-β signaling in cellular senescence and aging-related pathology
Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cell...
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MDPI AG
2020
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Online Access: | https://hdl.handle.net/1721.1/124915 |
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author | Tominaga, Kana Suzuki, Hiroshi I. |
author2 | Massachusetts Institute of Technology. Department of Biology |
author_facet | Massachusetts Institute of Technology. Department of Biology Tominaga, Kana Suzuki, Hiroshi I. |
author_sort | Tominaga, Kana |
collection | MIT |
description | Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cellular processes and has important roles in embryonic development, physiological tissue homeostasis, and various pathological conditions. TGF-β exerts potent growth inhibitory activities in various cell types, and multiple growth regulatory mechanisms have reportedly been linked to the phenotypes of cellular senescence and stem cell aging in previous studies. In addition, accumulated evidence has indicated a multifaceted association between TGF-β signaling and aging-associated disorders, including Alzheimer’s disease, muscle atrophy, and obesity. The findings regarding these diseases suggest that the impairment of TGF-β signaling in certain cell types and the upregulation of TGF-β ligands contribute to cell degeneration, tissue fibrosis, inflammation, decreased regeneration capacity, and metabolic malfunction. While the biological roles of TGF-β depend highly on cell types and cellular contexts, aging-associated changes are an important additional context which warrants further investigation to better understand the involvement in various diseases and develop therapeutic options. The present review summarizes the relationships between TGF-β signaling and cellular senescence, stem cell aging, and aging-related diseases. ©2019 keywords: transforming growth factor-β (TGF-β); cellular senescence; stem cell; aging |
first_indexed | 2024-09-23T12:48:50Z |
format | Article |
id | mit-1721.1/124915 |
institution | Massachusetts Institute of Technology |
last_indexed | 2024-09-23T12:48:50Z |
publishDate | 2020 |
publisher | MDPI AG |
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spelling | mit-1721.1/1249152022-10-01T11:16:31Z TGF-β signaling in cellular senescence and aging-related pathology Tominaga, Kana Suzuki, Hiroshi I. Massachusetts Institute of Technology. Department of Biology Koch Institute for Integrative Cancer Research at MIT Physical and Theoretical Chemistry Inorganic Chemistry Organic Chemistry Spectroscopy Molecular Biology Catalysis General Medicine Computer Science Applications Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cellular processes and has important roles in embryonic development, physiological tissue homeostasis, and various pathological conditions. TGF-β exerts potent growth inhibitory activities in various cell types, and multiple growth regulatory mechanisms have reportedly been linked to the phenotypes of cellular senescence and stem cell aging in previous studies. In addition, accumulated evidence has indicated a multifaceted association between TGF-β signaling and aging-associated disorders, including Alzheimer’s disease, muscle atrophy, and obesity. The findings regarding these diseases suggest that the impairment of TGF-β signaling in certain cell types and the upregulation of TGF-β ligands contribute to cell degeneration, tissue fibrosis, inflammation, decreased regeneration capacity, and metabolic malfunction. While the biological roles of TGF-β depend highly on cell types and cellular contexts, aging-associated changes are an important additional context which warrants further investigation to better understand the involvement in various diseases and develop therapeutic options. The present review summarizes the relationships between TGF-β signaling and cellular senescence, stem cell aging, and aging-related diseases. ©2019 keywords: transforming growth factor-β (TGF-β); cellular senescence; stem cell; aging 2020-04-29T02:09:41Z 2020-04-29T02:09:41Z 2019-10-10 Article http://purl.org/eprint/type/JournalArticle 1422-0067 https://hdl.handle.net/1721.1/124915 Tominaga, Kana, and Hiroshi I. Suzuki, "TGF-β signaling in cellular senescence and aging-related pathology." International Journal of Molecular Sciences 20 (2019): no. 5002 doi 10.3390/ijms20205002 ©2019 Author(s) 10.3390/ijms20205002 International Journal of Molecular Sciences Creative Commons Attribution 4.0 International license https://creativecommons.org/licenses/by/4.0/ application/pdf MDPI AG MDPI |
spellingShingle | Physical and Theoretical Chemistry Inorganic Chemistry Organic Chemistry Spectroscopy Molecular Biology Catalysis General Medicine Computer Science Applications Tominaga, Kana Suzuki, Hiroshi I. TGF-β signaling in cellular senescence and aging-related pathology |
title | TGF-β signaling in cellular senescence and aging-related pathology |
title_full | TGF-β signaling in cellular senescence and aging-related pathology |
title_fullStr | TGF-β signaling in cellular senescence and aging-related pathology |
title_full_unstemmed | TGF-β signaling in cellular senescence and aging-related pathology |
title_short | TGF-β signaling in cellular senescence and aging-related pathology |
title_sort | tgf β signaling in cellular senescence and aging related pathology |
topic | Physical and Theoretical Chemistry Inorganic Chemistry Organic Chemistry Spectroscopy Molecular Biology Catalysis General Medicine Computer Science Applications |
url | https://hdl.handle.net/1721.1/124915 |
work_keys_str_mv | AT tominagakana tgfbsignalingincellularsenescenceandagingrelatedpathology AT suzukihiroshii tgfbsignalingincellularsenescenceandagingrelatedpathology |