ArticleEuropean journal of applied physiology2012
Effect of lifestyle on age-related mitochondrial protein oxidation in mice cardiac muscle.
Article in European journal of applied physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Review
- Exercise Training Impacts Cardiac Mitochondrial Proteome Remodeling in Murine Urothelial Carcinoma.International journal of molecular sciences · 2018Article
- High activity before breeding improves reproductive performance by enhancing mitochondrial function and biogenesis.The Journal of experimental biology · 2018Article
- Exercise: Teaching myocytes new tricks.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Review
- Effect of reproductive ageing on pregnant mouse uterus and cervix.The Journal of physiology · 2017Article
- Mechanisms of exercise-induced cardioprotection.Physiology (Bethesda, Md.) · 2014Review
- Temporal patterns of tyrosine nitration in embryo heart development.Free radical biology & medicine · 2013Article
- Proteomic analyses of age related changes in A.BY/SnJ mouse hearts.Proteome science · 2013Article
- Cardiac aging and insulin resistance: could insulin/insulin-like growth factor (IGF) signaling be used as a therapeutic target?Current pharmaceutical design · 2013Review
- Protein carbonylation and metabolic control systems.Trends in endocrinology and metabolism: TEM · 2012Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the influence of lifestyle on aging-related changes in cardiac proteins' oxidative modifications profile. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young Y, old sedentary S, and old active A). The S and A mice were individually placed into standard cages and in cages with running wheels, respectively, for 23 months. Upon killing, heart mitochondrial fractions were obtained for the evaluation of general proteins oxidative modifications profile, the identification of preferential protein targets, and oxidative phosphorylation (OXPHOS) activity. We observed age-related cardiac muscle impairment, evidenced by decreased OXPHOS activity, paralleled by an increased protein susceptibility to carbonylation and nitration. Among the main targets to these posttranslational modifications we found mitochondrial proteins, mainly from OXPHOS complexes, MnSOD and enzymes from lipid metabolism. Lifelong sedentary behavior exacerbated the nitrative damage of mitochondrial proteins, paralleled by a statistically significant decrease of respiratory chain complexes II and III activities. In overall, our results highlight the determinant role of aging in cardiac muscle impairment, which is worsened by a sedentary lifestyle.
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Registered trials
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