Synthesis, Modification and Turnover of Proteins during Aging

Rattan, Suresh I. S.

doi:10.1007/978-1-4419-7002-2_1

Cited by 42 publications

(29 citation statements)

References 98 publications

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“…Branched chain amino acids, such as leucine, have been shown to boost signalling pathways that lead to increased protein translation in both humans and rodents [25, 26]. However, there is concern that these anabolic responses may be blunted in older people [27], raising the possibility that recommendations for protein intake should be increased [28]. There is good observational evidence that links low-protein intake to declining muscle mass [29], and supplementation with protein and/or amino acids should therefore have the potential to slow sarcopenic muscle loss.…”

Section: Managementmentioning

confidence: 99%

New horizons in the pathogenesis, diagnosis and management of sarcopenia

et al. 2013

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Sarcopenia is the age-related loss of skeletal muscle mass and function. It is now recognised as a major clinical problem for older people and research in the area is expanding exponentially. One of the most important recent developments has been convergence in the operational definition of sarcopenia combining measures of muscle mass and strength or physical performance. This has been accompanied by considerable progress in understanding of pathogenesis from animal models of sarcopenia. Well-described risk factors include age, gender and levels of physical activity and this knowledge is now being translated into effective management strategies including resistance exercise with recent interest in the additional role of nutritional intervention. Sarcopenia is currently a major focus for drug discovery and development although there remains debate about the best primary outcome measure for trials, and various promising avenues to date have proved unsatisfactory. The concept of ‘new tricks for old drugs’ is, however, promising, for example, there is some evidence that the angiotensin-converting enzyme inhibitors may improve physical performance. Future directions will include a deeper understanding of the molecular and cellular mechanisms of sarcopenia and the application of a lifecourse approach to understanding aetiology as well as to informing the optimal timing of interventions.

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Section: Managementmentioning

confidence: 99%

New horizons in the pathogenesis, diagnosis and management of sarcopenia

et al. 2013

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“…It is probably a safe generalisation to state that ageing in most organisms is accompanied by the accumulation of altered protein forms (Stadtman, 2001;Hipkiss, 2006a;Soskic et al, 2007;Rattan, 2010;Ahmed et al, 2010). Furthermore, much age-related disease is associated with proteostatic dysfunction (Ben-Zvi et al, 2009;Cenci et al, 2006;Douglas and Dillin, 2010).…”

Section: Introductionmentioning

confidence: 95%

Energy metabolism, proteotoxic stress and age-related dysfunction – Protection by carnosine

Hipkiss

2011

Molecular Aspects of Medicine

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“…120 With regards to protein degradation, the gradual shift from the proteasome pathway to the autophagic process has been observed during replicative senescence in a human I90 cell model of aging. 121 A myriad of evidence indicates a strong association between senescence and autophagy in various cell types.…”

Section: Autophagy and Agingmentioning

confidence: 99%

Macromolecular Degradation Systems and Cardiovascular Aging

Nakayama

Nishida

Otsu³

2016

Circulation Research

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7Cardiovascular aging or age-associated cardiovascular diseases include atherosclerosis, coronary artery disease, hypertension, heart failure, and atrial fibrillation. In addition, aged hearts are characterized by decreased contractility, impaired diastolic function, and atrium dilatation, indicating that both the functional and the morphological alterations that result in these diseases of the heart occur during the aging process. Abstract: Aging-related cardiovascular diseases are a rapidly increasing problem worldwide. Cardiac aging demonstrates progressive decline of diastolic dysfunction of ventricle and increase in ventricular and arterial stiffness accompanied by increased fibrosis stimulated by angiotensin II and proinflammatory cytokines. Reactive oxygen species and multiple signaling pathways on cellular senescence play major roles in the process. Aging is also associated with an alteration in steady state of macromolecular dynamics including a dysfunction of protein synthesis and degradation. Currently, impaired macromolecular degradation is considered to be closely related to enhanced inflammation and be involved in the process and mechanism of cardiac aging. Herein, we review the role and mechanisms of the degradation system of intracellular macromolecules in the process and pathophysiology of cardiovascular aging.

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Synthesis, Modification and Turnover of Proteins during Aging

Cited by 42 publications

References 98 publications

New horizons in the pathogenesis, diagnosis and management of sarcopenia

New horizons in the pathogenesis, diagnosis and management of sarcopenia

Energy metabolism, proteotoxic stress and age-related dysfunction – Protection by carnosine

Macromolecular Degradation Systems and Cardiovascular Aging

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