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      Mecanismos fisiopatológicos de la sarcopenia en la EPOC Translated title: Pathophysiological mechanism of sarcopenia in COPD

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          Abstract

          Resumen La sarcopenia es una enfermedad caracterizada por la pérdida de masa muscular, fuerza muscular y rendimiento físico, siendo la principal causa de fragilidad en los adultos mayores. La sarcopenia es altamente prevalente en individuos con enfermedad pulmonar obstructiva crónica (EPOC) que conduce a un mal pronóstico y una mayor mortalidad en esta población. La presencia de sarcopenia en la EPOC es probablemente el resultado de la interacción entre factores externos e internos como la inflamación sistémica, el estrés oxidativo y los polimorfismos genéticos, frecuentemente observados en individuos con esta enfermedad respiratoria. Esta revisión resume el conocimiento sobre los mecanismos patogénicos asociados con la sarcopenia en la EPOC.

          Translated abstract

          Sarcopenia is a disease characterized by loss of skeletal muscle, muscle strength and physical performance, being the major cause of frailty in the elderly. The sarcopenia is highly prevalent in individuals with Chronic obstructive pulmonary disease (COPD) leading to a poor prognosis and higher mortality in this population. The presence of sarcopenia in COPD is likely the result by the interaction between external and internal factors as systemic inflammation, oxidative stress and genetic polymorphisms, frequently observed in individuals with this respiratory disease. This review summarizes the current knowledge about the pathogenic mechanisms linking COPD with sarcopenia.

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          Welcome to the ICD‐10 code for sarcopenia

          Abstract The new ICD‐10‐CM (M62.84) code for sarcopenia represents a major step forward in recognizing sarcopenia as a disease. This should lead to an increase in availability of diagnostic tools and the enthusiasm for pharmacological companies to develop drugs for sarcopenia.
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            Oxidative stress in COPD.

            Oxidative stress is now recognized as a major predisposing factor in the pathogenesis of COPD. Existing therapies for COPD are ineffective at halting disease progression, with bronchodilators being the mainstay of pharmacotherapy, providing symptomatic relief only. It is, therefore, important for a better understanding of the underlying mechanisms by which oxidative stress drives disease pathogenesis to develop novel and more effective therapies. Antioxidant capacity in COPD is substantially reduced as a result of cigarette smoking and exacerbations, with oxidative stress persisting long after the cessation of cigarette smoking or exacerbation, due to the continued production of reactive oxygen species from endogenous sources. We discuss (1) how oxidative stress arises in the lung, (2) how it is neutralized, (3) what genetic factors may predispose to the development of COPD, and (4) how this impacts inflammation and autoimmunity in the development of emphysema and small airways disease. Finally, various strategies have been considered to neutralize the increased oxidative burden present in COPD. This review highlights why current antioxidant strategies have so far failed and what promising alternatives are on the horizon. Moreover, a number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.
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              Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials.

              Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                rcher
                Revista chilena de enfermedades respiratorias
                Rev. chil. enferm. respir.
                Sociedad Chilena de Enfermedades Respiratorias (Santiago, , Chile )
                0717-7348
                June 2019
                : 35
                : 2
                : 124-132
                Affiliations
                [3] Londrina Paraná orgnameUniversidade do Norte do Paraná Brazil
                [2] Paraná orgnameUniversidade Estadual de Londrina Brazil
                [1] Londrina Paraná orgnameUniversidade Estadual de Londrina Brazil
                Article
                S0717-73482019000200124
                22c38bee-e0e9-4cd4-8125-118036cc1fb4

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 69, Pages: 9
                Product

                SciELO Chile

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                Actualizaciones

                oxidative stress,pulmonary disease chronic obstructive,Sarcopenia,polimorfismos genéticos,inflamación,estrés oxidativo,enfermedad pulmonar obstructiva crónica,polymorphisms genetic,inflammation

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