@misc{10481/90834,
year = {2023},
month = {12},
url = {https://hdl.handle.net/10481/90834},
abstract = {Sarcopenia is an age-related condition that involves a progressive decline inmusclemass and
function, leading to increased risk of falls, frailty, andmortality. Although the exactmechanisms are not
fully understood, aging-related processes like inflammation, oxidative stress, reduced mitochondrial
capacity, and cell apoptosis contribute to this decline. Disruption of the circadian system with age
may initiate these pathways in skeletal muscle, preceding the onset of sarcopenia. At present, there
is no pharmacological treatment for sarcopenia, only resistance exercise and proper nutrition may
delay its onset. Melatonin, derived from tryptophan, emerges as an exceptional candidate for treating
sarcopenia due to its chronobiotic, antioxidant, and anti-inflammatory properties. Its impact on
mitochondria and organelle, where it is synthesized and crucial in aging skeletal muscle, further
highlights its potential. In this review, we discuss the influence of clock genes in muscular aging, with
special reference to peripheral clock genes in the skeletal muscle, as well as their relationship with
melatonin, which is proposed as a potential therapy against sarcopenia.},
organization = {Instituto de Salud Carlos III, grant numbers PI19-01372
and CB/10/00238},
organization = {FPU fellowship from the Ministerio de Universidades,
Spain},
organization = {PFIS fellowship from the Instituto de Salud Carlos III},
publisher = {MDPI},
keywords = {Aging},
keywords = {Chronodisruption},
keywords = {Clock genes},
title = {From Chronodisruption to Sarcopenia: The Therapeutic Potential of Melatonin},
doi = {10.3390/biom13121779},
author = {Fernández Martínez, José and Ramírez Casas, Yolanda and Yang, Yang and Aranda Martínez, Paula and Martínez Ruiz, Laura and Escames Rosa, Germaine and Acuña Castroviejo, Darío},
}