The Role of Autophagy in Muscle Health
New ways to keep our muscles strong - even as we get older
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When maintaining cells, i.e. cell purification, a crucial mechanism that creates a balance between breakdown and renewal. While a surplus of autophagy can increase tissue degeneration, a lack of autophagy also contributes to degenerative processes. The interplay between AMPK-metabolic path that promotes autophagy, and the mTOR-Metabolic path that inhibits them underlines the complexity of regulating this process.
Within the spectrum of autophagy, mitophagy, which is primarily controlled by PGC-1α and targets dysfunctional mitochondria for degradation, is a focus. Despite its complexity, the exact biochemical processes of autophagy have not yet been fully elucidated, and research is ongoing.
In a study with 575 participants, mostly of European origin and an average age of 75.9 years, the relationship between the expression of genes associated with autophagy and functional parameters was investigated. The RNA sequencing of 260 selected genes involving autophagy, mitophagy and are linked to the mTOR signaling pathway, revealed interesting correlations with mitochondrial function and physical performance, in particular the 400-meter running speed.
Interestingly, genes that are directly involved in autophagy did not seem to have much effect on the ability of our muscles to function as we age. Other genes such as Foxo1, which help regulate autophagy, however, showed unexpected links. Instead of helping, they appeared to be linked to poorer muscle function.
In contrast, genes related to the way our bodies use energy and manage our mitochondria were linked to better muscle function. Influencing the mTOR signaling path, which controls cell growth, also proved to be promising for improving muscle performance in older people.
These findings question everything we thought we knew about Foxo1 so far. It appears that when autophagy isn't working properly, our bodies try to compensate by booting up Foxo1.
By interfering with the mTOR pathway, new ways may be found to keep our muscles strong even in old age. This opens up exciting possibilities for new therapies to help older people stay fit and healthy.
References
Coen, P.M., Huo, Z., Tranah, G.J., Barnes, H.N., Zhang, X., Wolff, C.A., Wu, K., Cawthon, P.M., Hepple, R.T., Toledo, F.G.S., Evans, D.S., Santiago-Fernández, O., Cuervo, A.M., Kritchevsky, S.B., Newman, A.B., Cummings, S.R., & Esser, K.A. (2024). Autophagy gene expression in skeletal muscle of older individuals is associated with physical performance, muscle volume and mitochondrial function in the study of muscle, mobility and aging (SOMMA). Aging Cell, 00, e14118. https://doi.org/10.1111/acel.14118
Publiziert
1.7.2024
Kategorie
Science
Experte
Scientific Terms
Autophagy
From ancient Greek αφααγоs autóphagos 'eating oneself. '
A normal and orderly process of breaking down and recycling damaged cell components.
Mitophagy
From ancient Greek μmítos, German 'thread' and ancient Greek φαγεν phagein, German 'eat'
Mitophagy is a process by which damaged mitochondria are removed from the cell, which promotes the growth and maintenance of healthy mitochondria.
Mitochondrion
Mitochondria are often referred to as the cell's powerhouse and break down nutrients to generate energy in a process called cellular respiration. They contain their own circular genome.
When maintaining cells, i.e. cell purification, a crucial mechanism that creates a balance between breakdown and renewal. While a surplus of autophagy can increase tissue degeneration, a lack of autophagy also contributes to degenerative processes. The interplay between AMPK-metabolic path that promotes autophagy, and the mTOR-Metabolic path that inhibits them underlines the complexity of regulating this process.
Within the spectrum of autophagy, mitophagy, which is primarily controlled by PGC-1α and targets dysfunctional mitochondria for degradation, is a focus. Despite its complexity, the exact biochemical processes of autophagy have not yet been fully elucidated, and research is ongoing.
In a study with 575 participants, mostly of European origin and an average age of 75.9 years, the relationship between the expression of genes associated with autophagy and functional parameters was investigated. The RNA sequencing of 260 selected genes involving autophagy, mitophagy and are linked to the mTOR signaling pathway, revealed interesting correlations with mitochondrial function and physical performance, in particular the 400-meter running speed.
Interestingly, genes that are directly involved in autophagy did not seem to have much effect on the ability of our muscles to function as we age. Other genes such as Foxo1, which help regulate autophagy, however, showed unexpected links. Instead of helping, they appeared to be linked to poorer muscle function.
In contrast, genes related to the way our bodies use energy and manage our mitochondria were linked to better muscle function. Influencing the mTOR signaling path, which controls cell growth, also proved to be promising for improving muscle performance in older people.
These findings question everything we thought we knew about Foxo1 so far. It appears that when autophagy isn't working properly, our bodies try to compensate by booting up Foxo1.
By interfering with the mTOR pathway, new ways may be found to keep our muscles strong even in old age. This opens up exciting possibilities for new therapies to help older people stay fit and healthy.
Experte
Referenzen
Coen, P.M., Huo, Z., Tranah, G.J., Barnes, H.N., Zhang, X., Wolff, C.A., Wu, K., Cawthon, P.M., Hepple, R.T., Toledo, F.G.S., Evans, D.S., Santiago-Fernández, O., Cuervo, A.M., Kritchevsky, S.B., Newman, A.B., Cummings, S.R., & Esser, K.A. (2024). Autophagy gene expression in skeletal muscle of older individuals is associated with physical performance, muscle volume and mitochondrial function in the study of muscle, mobility and aging (SOMMA). Aging Cell, 00, e14118. https://doi.org/10.1111/acel.14118
Publiziert
1.7.2024
Kategorie
Science
Wissenschaftliche Begriffe
Autophagy
From ancient Greek αφααγоs autóphagos 'eating oneself. '
A normal and orderly process of breaking down and recycling damaged cell components.
Mitophagy
From ancient Greek μmítos, German 'thread' and ancient Greek φαγεν phagein, German 'eat'
Mitophagy is a process by which damaged mitochondria are removed from the cell, which promotes the growth and maintenance of healthy mitochondria.
Mitochondrion
Mitochondria are often referred to as the cell's powerhouse and break down nutrients to generate energy in a process called cellular respiration. They contain their own circular genome.
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