Details
| Original language | English |
|---|---|
| Pages (from-to) | 14883-14895 |
| Number of pages | 13 |
| Journal | Journal of Celluar Physiology |
| Volume | 234 |
| Issue number | 9 |
| Early online date | 12 Feb 2019 |
| Publication status | Published - 24 May 2019 |
Abstract
Aging is one of the risk factors for the development of low-grade inflammation morbidities, such as several types of cancer and neurodegenerative diseases, due to changes in the metabolism, hormonal secretion, and immunosenescence. The senescence of the immune system leads to improper control of infections and tissue damage increasing age-related diseases. One of the mechanisms that maintain cellular homeostasis is autophagy, a cell-survival mechanism, and it has been proposed as one of the most powerful antiaging therapies. Regular exercise can reestablish autophagy, probably through AMP-activated protein kinase activation, and help in reducing the age-related senescence diseases. Therefore, in this study, we discuss the effects of exercise training in immunosenescence and autophagy, preventing the two main age-related disease, cancer and neurodegeneration.
Keywords
- autophagy, cancer, exercise, immunosenescence, neurodegeneration
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Physiology
- Biochemistry, Genetics and Molecular Biology(all)
- Clinical Biochemistry
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology
Sustainable Development Goals
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In: Journal of Celluar Physiology, Vol. 234, No. 9, 24.05.2019, p. 14883-14895.
Research output: Contribution to journal › Review article › Research › peer review
}
TY - JOUR
T1 - Regulation of autophagy as a therapy for immunosenescence-driven cancer and neurodegenerative diseases: The role of exercise
AU - Batatinha, Helena Angelica Pereira
AU - Diniz, Tiego Aparecido
AU - de Souza Teixeira, Alexandre Abilio
AU - Krüger, K.
AU - Neto, Jose Cesar Rosa
N1 - Funding Information: Fundação de Amparo à Pesquisa do Estado de São Paulo, Grant/Award Number: 2016/ 10561‐8; Sao Paulo Research Foundation (FAPESP), Grant/Award Number: 2016/ 01409‐8
PY - 2019/5/24
Y1 - 2019/5/24
N2 - Aging is one of the risk factors for the development of low-grade inflammation morbidities, such as several types of cancer and neurodegenerative diseases, due to changes in the metabolism, hormonal secretion, and immunosenescence. The senescence of the immune system leads to improper control of infections and tissue damage increasing age-related diseases. One of the mechanisms that maintain cellular homeostasis is autophagy, a cell-survival mechanism, and it has been proposed as one of the most powerful antiaging therapies. Regular exercise can reestablish autophagy, probably through AMP-activated protein kinase activation, and help in reducing the age-related senescence diseases. Therefore, in this study, we discuss the effects of exercise training in immunosenescence and autophagy, preventing the two main age-related disease, cancer and neurodegeneration.
AB - Aging is one of the risk factors for the development of low-grade inflammation morbidities, such as several types of cancer and neurodegenerative diseases, due to changes in the metabolism, hormonal secretion, and immunosenescence. The senescence of the immune system leads to improper control of infections and tissue damage increasing age-related diseases. One of the mechanisms that maintain cellular homeostasis is autophagy, a cell-survival mechanism, and it has been proposed as one of the most powerful antiaging therapies. Regular exercise can reestablish autophagy, probably through AMP-activated protein kinase activation, and help in reducing the age-related senescence diseases. Therefore, in this study, we discuss the effects of exercise training in immunosenescence and autophagy, preventing the two main age-related disease, cancer and neurodegeneration.
KW - autophagy
KW - cancer
KW - exercise
KW - immunosenescence
KW - neurodegeneration
UR - http://www.scopus.com/inward/record.url?scp=85061439585&partnerID=8YFLogxK
U2 - 10.1002/jcp.28318
DO - 10.1002/jcp.28318
M3 - Review article
VL - 234
SP - 14883
EP - 14895
JO - Journal of Celluar Physiology
JF - Journal of Celluar Physiology
IS - 9
ER -