Direct or indirect regulation of muscle protein synthesis by energy status?

Moinard, Christophe; Fontaine, Éric

doi:10.1016/j.clnu.2020.07.015

Cited by 6 publications

(4 citation statements)

References 21 publications

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“…By its thermodynamic action, CIT may decrease activation energies of one or several ATP (and GTP)‐consuming reactions involved in cell and, in fine, preserve cell from death. 54 Alterations of the cellular energy dynamics with reduced ATP have been reported in H 2 O 2 ‐treated ARPE‐19 cells 55 and are classically observed during oxidative stress. Thus, we assume that the thermodynamic properties of CIT could also explain in part its protective effect.…”

Section: Discussionmentioning

confidence: 98%

“…In such conditions, many reactions (requiring high levels energy in cells) are no longer possible and it may lead to cell death. By its thermodynamic action, CIT may decrease activation energies of one or several ATP (and GTP)‐consuming reactions involved in cell and, in fine, preserve cell from death 54 . Alterations of the cellular energy dynamics with reduced ATP have been reported in H 2 O 2 ‐treated ARPE‐19 cells 55 and are classically observed during oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

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Citrulline protects human retinal pigment epithelium from hydrogen peroxide and iron/ascorbate induced damages

Hassel

Couchet

Jacquemot

et al. 2022

J Cellular Molecular Medi

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Oxidative stress appears to play an important role during ageing of the retina and in the pathophysiology of retinal diseases, such as age-related macular degeneration (ARMD). [1][2][3] The retinal pigment epithelium (RPE), localized between the choroid and the neural retina, is particularly vulnerable to oxidative damage caused by reactive oxygen species (ROS). 4 Hydrogen peroxide (H 2 O 2 ) is a ROS generated during RPE phagocytosis of photoreceptor outer segments 5,6 and during light irradiation of melanin present in the RPE. 7 This oxidant is also produced by the photo-excited lipofuscin that accumulates with age in the RPE, and its accumulation is associated with ARMD. 8 Also, it has been reported that iron levels increase in RPE during ageing and that age-dependent iron accumulation is accelerated in patients with ARMD. [9][10][11] Additionally, accumulation of iron can be toxic to the RPE. Indeed, the increase of intracellular ferrous iron produces hydroxyl and lipid alkoxyl radicals through the Fenton reaction, leading to lipid peroxidation and protein oxidation. 12,13

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Citrulline protects human retinal pigment epithelium from hydrogen peroxide and iron/ascorbate induced damages

Hassel

Couchet

Jacquemot

et al. 2022

J Cellular Molecular Medi

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“…Finally, during ischemia-reperfusion, the decrease in ATP/ADP ratio slowed reactions requiring high energy levels. By thermodynamic action, previously described as a decrease in the energy activation levels of one or several ATP-consuming reactions [ 68 , 69 ], citrulline may protect against cardiomyocyte death.…”

Section: Discussionmentioning

confidence: 99%

L-Citrulline Supplementation Reduces Blood Pressure and Myocardial Infarct Size under Chronic Intermittent Hypoxia, a Major Feature of Sleep Apnea Syndrome

et al. 2022

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Intermittent hypoxia (IH) is a landmark of obstructive sleep apnea (OSA) at the core of the cardiovascular consequences of OSA. IH triggers oxidative stress, a major underlying mechanism for elevated blood pressure (BP) and increased infarct size. L-citrulline is an amino acid that has been demonstrated to be protective of the cardiovascular system and exert pleiotropic effects. Therefore, we tested the impact of citrulline supplementation on IH-induced increase in BP and infarct size. Four groups of rats exposed to normoxia (N) or IH [14 days (d), 8 h/day, 30 s-O2 21%/30 s-O2 5%] and were supplemented or not with citrulline (1 g·kg−1·d−1). After 14 d, BP was measured, and hearts were submitted to global ischemia-reperfusion to measure infarct size. Histological and biochemical analyses were conducted on hearts and aorta to assess oxidative stress. Citrulline significantly reduced BP (–9.92%) and infarct size (–18.22%) under IH only. In the aorta, citrulline supplementation significantly decreased superoxide anion and nitrotyrosine levels under IH and abolished the IH-induced decrease in nitrite. Citrulline supplementation significantly decreased myocardial superoxide anion levels and xanthine oxidase enzyme activity under IH. Citrulline shows a cardioprotective capacity by limiting IH-induced pro-oxidant activity. Our results suggest that citrulline might represent a new pharmacological strategy in OSA patients with high cardiovascular risk.

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“…In this respect, it is noteworthy that the causal relation between decreased oxidative capacity and perturbed proteostasis in aged skeletal muscle remains uncertain. Explicitly or implicitly, it is often argued that the rate of protein synthesis is lowered in sarcopenia because dysfunctional mitochondria are unable to sufficiently sustain this and other anabolic processes energetically, [20][21][22][23]86 but it is equally conceivable that the decreased oxidative phosphorylation capacity is an adaptation to lowered ATP demand from the depressed anabolism that follows from insulin and anabolic resistance 69,87 (Figure 2).…”

Section: Mitochondrial Bioenergeticsmentioning

confidence: 99%

Mitochondrial involvement in sarcopenia

Affourtit,

Carré

2024

Acta Physiologica

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Sarcopenia lowers the quality‐of‐life for millions of people across the world, as accelerated loss of skeletal muscle mass and function contributes to both age‐ and disease‐related frailty. Physical activity remains the only proven therapy for sarcopenia to date, but alternatives are much sought after to manage this progressive muscle disorder in individuals who are unable to exercise. Mitochondria have been widely implicated in the etiology of sarcopenia and are increasingly suggested as attractive therapeutic targets to help restore the perturbed balance between protein synthesis and breakdown that underpins skeletal muscle atrophy. Reviewing current literature, we note that mitochondrial bioenergetic changes in sarcopenia are generally interpreted as intrinsic dysfunction that renders muscle cells incapable of making sufficient ATP to fuel protein synthesis. Based on the reported mitochondrial effects of therapeutic interventions, however, we argue that the observed bioenergetic changes may instead reflect an adaptation to pathologically decreased energy expenditure in sarcopenic muscle. Discrimination between these mechanistic possibilities will be crucial for improving the management of sarcopenia.

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Direct or indirect regulation of muscle protein synthesis by energy status?

Cited by 6 publications

References 21 publications

Citrulline protects human retinal pigment epithelium from hydrogen peroxide and iron/ascorbate induced damages

Citrulline protects human retinal pigment epithelium from hydrogen peroxide and iron/ascorbate induced damages

L-Citrulline Supplementation Reduces Blood Pressure and Myocardial Infarct Size under Chronic Intermittent Hypoxia, a Major Feature of Sleep Apnea Syndrome

Mitochondrial involvement in sarcopenia

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