Sarcopenia: Molecular Pathways and Potential Targets for Intervention

Pascual-Fernández, Jorge; Fernandez‐Montero, Alejandro; Córdova-Martínez, Alfredo; Pastor, Diego; Martínez-Rodríguez, Alejandro; Roche, Enrique

doi:10.3390/ijms21228844

Cited by 61 publications

(36 citation statements)

References 110 publications

(160 reference statements)

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“…Despite the fact that the effect of Ang-(1-7) has not been directly assayed in SO, the mechanisms involved in muscle mass regulation include decreased protein degradation, prevention of Os, apoptosis, and mitochondrial dysfunction. These features are separately present in skeletal muscle from obese and aged mice [145][146][147].…”

Section: Animal Modelsmentioning

confidence: 99%

The Critical Role of Oxidative Stress in Sarcopenic Obesity

González

Simón

Achiardi

et al. 2021

Oxidative Medicine and Cellular Longevity

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Sarcopenic obesity (SO) is a combination of obesity and sarcopenia that primarily develops in older people. Patients with SO have high fat mass, low muscle mass, low muscle strength, and low physical function. SO relates to metabolic syndrome and an increased risk of morbimortality. The prevalence of SO varies because of lacking consensus criteria regarding its definition and the methodological difficulty in diagnosing sarcopenia and obesity. SO includes systemic alterations such as insulin resistance, increased proinflammatory cytokines, age-associated hormonal changes, and decreased physical activity at pathophysiological levels. Interestingly, these alterations are influenced by oxidative stress, which is a critical factor in altering muscle function and the generation of metabolic dysfunctions. Thus, oxidative stress in SO alters muscle mass, the signaling pathways that control it, satellite cell functions, and mitochondrial and endoplasmic reticulum activities. Considering this background, our objectives in this review are to describe SO as a highly prevalent condition and look at the role of oxidative stress in SO pathophysiology.

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Section: Animal Modelsmentioning

confidence: 99%

The Critical Role of Oxidative Stress in Sarcopenic Obesity

González

Simón

Achiardi

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Most of our understanding of molecular and cellular mechanisms in myofibers and the muscle scaffold during aging stem from work done on laboratory animals. For a detailed account on myogenic mechanisms in the sarcopenia processes, we refer to some recent reviews (Larsson et al, 2019;Christian and Benian, 2020;Pascual-Fernández et al, 2020). Briefly, early studies on sarcopenia (previously referred to as old-age-muscleatrophy or senile-muscle-atrophy) in laboratory small rodents and humans revealed that aging is accompanied by a loss of myofibers, atrophy preferentially affecting fast twitch (type II) myofibers, and a fiber type grouping-features that increase with advancing chronological age.…”

Section: The Sarcopenic Skeletal Musclementioning

confidence: 99%

Sarcopenia: What Is the Origin of This Aging-Induced Disorder?

Gustafsson

Ulfhake

2021

Front. Genet.

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We here review the loss of muscle function and mass (sarcopenia) in the framework of human healthspan and lifespan, and mechanisms involved in aging. The rapidly changing composition of the human population will impact the incidence and the prevalence of aging-induced disorders such as sarcopenia and, henceforth, efforts to narrow the gap between healthspan and lifespan should have top priority. There are substantial knowledge gaps in our understanding of aging. Heritability is estimated to account for only 25% of lifespan length. However, as we push the expected lifespan at birth toward those that we consider long-lived, the genetics of aging may become increasingly important. Linkage studies of genetic polymorphisms to both the susceptibility and aggressiveness of sarcopenia are still missing. Such information is needed to shed light on the large variability in clinical outcomes between individuals and why some respond to interventions while others do not. We here make a case for the concept that sarcopenia has a neurogenic origin and that in manifest sarcopenia, nerve and myofibers enter into a vicious cycle that will escalate the disease progression. We point to gaps in knowledge, for example the crosstalk between the motor axon, terminal Schwann cell, and myofiber in the denervation processes that leads to a loss of motor units and muscle weakness. Further, we argue that the operational definition of sarcopenia should be complemented with dynamic metrics that, along with validated biomarkers, may facilitate early preclinical diagnosis of individuals vulnerable to develop advanced sarcopenia. We argue that preventive measures are likely to be more effective to counter act aging-induced disorders than efforts to treat manifest clinical conditions. To achieve compliance with a prescription of preventive measures that may be life-long, we need to identify reliable predictors to design rational and convincing interventions.

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“…Increases in these enzymes may represent an index of necrosis and tissue damage following acute as well as chronic muscle injuries [ 35 ]. Therefore, considering these muscle markers as indicators of muscle status, they are very useful to follow the evolution of sarcopenia just using the regular blood analysis performed usually in laboratories and health centres [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

L-Citrulline Supplementation and Exercise in the Management of Sarcopenia

et al. 2021

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Sarcopenia is a process associated to aging. Persistent inflammation and oxidative stress in muscle favour muscle wasting and decreased ability to perform physical activity. Controlled exercise can optimize blood flux and moderate the production of reactive oxygen species. Therefore, supplements that can work as a vasodilators and control oxidative stress, might be beneficial for active elders. In this context, we have tested citrulline supplementation in a group of 44 participants aged from 60–73 years that followed a physical activity program adapted to their age and capacities. Volunteers were divided in two groups: placebo (n = 22) and citrullline supplemented (n = 22). Different physical tests and blood extractions were performed at the beginning and at the end of intervention (six weeks). Strength and endurance showed a tendency to increase in the citrulline supplemented group, with no significant differences respect to placebo. However, walking speed in the citrulline supplemented group improved significantly compared to placebo. Markers of muscle damage as well as circulating levels of testosterone, cortisol and vitamin D showed no significant changes, but a tendency to improve at the end of intervention in the supplemented group compared to placebo. Additional studies are necessary to confirm the effect of citrulline supplementation in sarcopenia delay.

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Sarcopenia: Molecular Pathways and Potential Targets for Intervention

Cited by 61 publications

References 110 publications

The Critical Role of Oxidative Stress in Sarcopenic Obesity

The Critical Role of Oxidative Stress in Sarcopenic Obesity

Sarcopenia: What Is the Origin of This Aging-Induced Disorder?

L-Citrulline Supplementation and Exercise in the Management of Sarcopenia

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