Role of melatonin in the regulation of autophagy and mitophagy: A review

Coto‐Montes, Ana; Boga, José Antonio; Rosales-Corral, Sergio; Fuentes-Broto, Lorena; Tan, Dun Xian; Reíter, Russel J.

doi:10.1016/j.mce.2012.04.009

Cited by 142 publications

(132 citation statements)

References 201 publications

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“…The influence of melatonin on autophagy seems well conserved since this association also has been found in plants [200,201]. Based on published data, Coto-Montes et al [202] speculated that a specific autophagy, i.e., mitophagy, could also be influenced by melatonin. This speculation is supported by the observations summarized herein that melatonin indeed targets the process of mitophagy.…”

Section: Melatonin Regulates Mitochondrial Dynamicsmentioning

confidence: 93%

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Tan

Manchester

Qin

et al. 2016

IJMS

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Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s). Melatonin protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting the mitochondrial permeability transition pore (MPTP), and activating uncoupling proteins (UCPs). Thus, melatonin maintains the optimal mitochondrial membrane potential and preserves mitochondrial functions. In addition, mitochondrial biogenesis and dynamics is also regulated by melatonin. In most cases, melatonin reduces mitochondrial fission and elevates their fusion. Mitochondrial dynamics exhibit an oscillatory pattern which matches the melatonin circadian secretory rhythm in pinealeocytes and probably in other cells. Recently, melatonin has been found to promote mitophagy and improve homeostasis of mitochondria.

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Section: Melatonin Regulates Mitochondrial Dynamicsmentioning

confidence: 93%

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Tan

Manchester

Qin

et al. 2016

IJMS

Self Cite

312

256

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“…Melatonin, in its role as a homeostasis stabilizer, has been shown to induce [84] or reduce [85] autophagy. In relation to muscle, melatonin is highly versatile molecule and either induces autophagy [86] or inhibits it [87], depending on pathological processes involved, since oxidative stress has a close relationship with autophagy.…”

Section: Cellular Impact Of Sarcopeniamentioning

confidence: 99%

Melatonin as a Potential Agent in the Treatment of Sarcopenia

Coto‐Montes

Boga

Tan

et al. 2016

IJMS

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Considering the increased speed at which the world population is aging, sarcopenia could become an epidemic in this century. This condition currently has no means of prevention or treatment. Melatonin is a highly effective and ubiquitously acting antioxidant and free radical scavenger that is normally produced in all organisms. This molecule has been implicated in a huge number of biological processes, from anticonvulsant properties in children to protective effects on the lung in chronic obstructive pulmonary disease. In this review, we summarize the data which suggest that melatonin may be beneficial in attenuating, reducing or preventing each of the symptoms that characterize sarcopenia. The findings are not limited to sarcopenia, but also apply to osteoporosis-related sarcopenia and to age-related neuromuscular junction dysfunction. Since melatonin has a high safety profile and is drastically reduced in advanced age, its potential utility in the treatment of sarcopenic patients and related dysfunctions should be considered.

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“…These stimuli may trigger different cellular responses including changes in autophagy (García-Macia et al, 2014). Autophagy is considered a specialized form of lysosomal proteolysis, where a portion of the cytoplasm or entire organelles are sequestered into double-membrane vesicles known as autophagosomes, which then fuse with lysosomes, resulting in the degradation of their contents by lysosomal cathepsins (Caballero and Coto-Montes, 2012;Coto-Montes et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Effect of animal mixing as a stressor on biomarkers of autophagy and oxidative stress during pig muscle maturation

Rubio-González

Potes

Illán-Rodríguez

et al. 2015

Animal

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The objective of this work was to study the postmortem evolution of potential biomarkers of autophagy (Beclin 1, LC3-II/LC3-I ratio) and oxidative stress (total antioxidant activity, TAA; superoxide dismutase activity, SOD and catalase activity, CAT) in the Longissimus dorsi muscle of entire male ((Large White × Landrace) × Duroc) pigs subjected to different management treatments that may promote stress, such as mixing unfamiliar animals at the farm and/or during transport and lairage before slaughter. During the rearing period at the farm, five animals were never mixed after the initial formation of the experimental groups (unmixed group at the farm, UF), whereas 10 animals were subjected to a common routine of being mixed with unfamiliar animals (mixed group at the farm, MF). Furthermore, two different treatments were used during the transport and lairage before slaughter: 10 pigs were not mixed (unmixed group during transport and lairage, UTL), whereas five pigs were mixed with unfamiliar animals on the lorry and during lairage (mixed group during transport and lairage, MTL). These mixing treatments were then combined into three pre-slaughter treatments -namely, UF-UTL, MF-UTL and MF-MTL. The results show that MF-UTL and MF-MTL increased significantly the muscle antioxidant defense (TAA, SOD and CAT) at short postmortem times (4 and 8 h; P < 0.001), followed by an earlier depletion of the antioxidant activity at 24 h postmortem (P < 0.05). We also found that mixing unfamiliar animals, both at the farm and during transport and lairage, triggers postmortem muscle autophagy, which showed an earlier activation (higher expression of Beclin 1 and LC3-II/LC3-I ratio at 4 h postmortem followed by a decreasing pattern of this ratio along first 24 h postmortem) in the muscle tissues of animals from the MF-UTL and MF-MTL groups, as an adaptive strategy of the muscle cells for counteracting induced stress. From these results, we propose that monitoring the evolution of the main biomarkers of autophagy (Beclin 1, LC3-II/LC3-I ratio) and muscle antioxidant defense (TAA, SOD, CAT) in the muscle tissue within the first 24 h postmortem may help the detection of animal stress and its potential effect on the postmortem muscle metabolism.

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Role of melatonin in the regulation of autophagy and mitophagy: A review

Cited by 142 publications

References 201 publications

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Melatonin as a Potential Agent in the Treatment of Sarcopenia

Effect of animal mixing as a stressor on biomarkers of autophagy and oxidative stress during pig muscle maturation

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