Barreiro Portela, Esther2016-06-212016-06-212016Barreiro A. Role of protein carbonylation in skeletal muscle mass loss associated with chronic conditions. Proteomes. 2016;4(2):18. DOI: 10.3390/proteomes40200182227-7382http://hdl.handle.net/10230/26950Muscle dysfunction, characterized by a reductive remodeling of muscle fibers, is a commonsystemic manifestation in highly prevalent conditions such as chronic heart failure (CHF), chronicobstructive pulmonary disease (COPD), cancer cachexia, and critically ill patients. Skeletal muscledysfunction and impaired muscle mass may predict morbidity and mortality in patients with chronicdiseases, regardless of the underlying condition. High levels of oxidants may alter function andstructure of key cellular molecules such as proteins, DNA, and lipids, leading to cellular injuryand death. Protein oxidation including protein carbonylation was demonstrated to modify enzymeactivity and DNA binding of transcription factors, while also rendering proteins more prone toproteolytic degradation. Given the relevance of protein oxidation in the pathophysiology of manychronic conditions and their comorbidities, the current review focuses on the analysis of differentstudies in which the biological and clinical significance of the modifications induced by reactivecarbonyls on proteins have been explored so far in skeletal muscles of patients and animal models ofchronic conditions such as COPD, disuse muscle atrophy, cancer cachexia, sepsis, and physiologicalaging. Future research will elucidate the specific impact and sites of reactive carbonyls on muscleprotein content and function in human conditionsapplication/pdfeng©2016 by the author; licensee MDPI, Basel, Switzerland. This article is an open accessarticle distributed under the terms and conditions of the Creative Commons Attribution(CC-BY) license http://creativecommons.org/licenses/by/4.0/)Oxidació fisiològicaMalalts crònicsAparell locomotor -- Malaltiesinfo:eu-repo/semantics/articlehttp://dx.doi.org/10.3390/proteomes4020018info:eu-repo/semantics/openAccess