TY - JOUR
T1 - Update on mitochondria and muscle aging: All wrong roads lead to sarcopenia
AU - Picca, Anna
AU - Calvani, Riccardo
AU - Bossola, Maurizio
AU - Allocca, Elena
AU - Menghi, Amerigo
AU - Pesce, Vito
AU - Lezza, Angela Maria Serena
AU - Bernabei, Roberto
AU - Landi, Francesco
AU - Marzetti, Emanuele
PY - 2018
Y1 - 2018
N2 - Sarcopenia is a well-known geriatric syndrome that has been endorsed over the years as a biomarker allowing for the discrimination, at a clinical level, of biological from chronological age. Multiple candidate mechanisms have been linked to muscle degeneration during sarcopenia. Among them, there is wide consensus on the central role played by the loss of mitochondrial integrity in myocytes, secondary to dysfunctional quality control mechanisms. Indeed, mitochondria establish direct or indirect contacts with other cellular components (e.g. endoplasmic reticulum, peroxisomes, lysosomes/vacuoles) as well as the extracellular environment through the release of several biomolecules. The functional implications of these interactions in the context of muscle physiology and sarcopenia are not yet fully appreciated and represent a promising area of investigation. Here, we present an overview of recent findings concerning the interrelation between mitochondrial quality control processes, inflammation and the metabolic regulation of muscle mass in the pathogenesis of sarcopenia highlighting those pathways that may be exploited for developing preventive and therapeutic interventions against muscle aging.
AB - Sarcopenia is a well-known geriatric syndrome that has been endorsed over the years as a biomarker allowing for the discrimination, at a clinical level, of biological from chronological age. Multiple candidate mechanisms have been linked to muscle degeneration during sarcopenia. Among them, there is wide consensus on the central role played by the loss of mitochondrial integrity in myocytes, secondary to dysfunctional quality control mechanisms. Indeed, mitochondria establish direct or indirect contacts with other cellular components (e.g. endoplasmic reticulum, peroxisomes, lysosomes/vacuoles) as well as the extracellular environment through the release of several biomolecules. The functional implications of these interactions in the context of muscle physiology and sarcopenia are not yet fully appreciated and represent a promising area of investigation. Here, we present an overview of recent findings concerning the interrelation between mitochondrial quality control processes, inflammation and the metabolic regulation of muscle mass in the pathogenesis of sarcopenia highlighting those pathways that may be exploited for developing preventive and therapeutic interventions against muscle aging.
KW - Inflammation
KW - Mitochondrial biogenesis
KW - Mitochondrial proteostasis
KW - Mitochondrial quality control
KW - Mitophagy
KW - Muscle wasting
KW - Inflammation
KW - Mitochondrial biogenesis
KW - Mitochondrial proteostasis
KW - Mitochondrial quality control
KW - Mitophagy
KW - Muscle wasting
UR - http://hdl.handle.net/10807/220789
U2 - 10.1515/hsz-2017-0331
DO - 10.1515/hsz-2017-0331
M3 - Article
SN - 1431-6730
VL - 399
SP - 421
EP - 436
JO - Biological Chemistry
JF - Biological Chemistry
ER -