Molecular signatures of longevity: Insights from cross-species comparative studies

Ma, Siming; Gladyshev, Vadim N.

doi:10.1016/j.semcdb.2017.08.007

Cited by 90 publications

(83 citation statements)

References 111 publications

(227 reference statements)

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“…This strong correlation with lifespan (p < 0.0001) only held for cytosolic proteins despite increased N-acetylation of proteins in the mitochondrial matrix [35]. Thus, low stoichiometry lysine N-acylation, not associated with any particular acylation site, may be linked to the wide variation in maximum lifespan between species [45,46].…”

Section: Low Stoichiometry Protein Acylation Is a Stress With Detrimementioning

confidence: 91%

The Causes and Consequences of Nonenzymatic Protein Acylation

James

Smith

et al. 2018

Trends in Biochemical Sciences

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Thousands of protein acyl modification sites have now been identified in vivo. However, at most sites the acylation stoichiometry is low, making functional enzyme-driven regulation in the majority of cases unlikely. As unmediated acylation can occur on the surface of proteins when acyl-CoA thioesters react with nucleophilic cysteine and lysine residues, slower nonenzymatic processes likely underlie most protein acylation. Here, we review how nonenzymatic acylation of nucleophilic lysine and cysteine residues occurs; the factors that enhance acylation at particular sites; and the strategies that have evolved to limit protein acylation. We conclude that protein acylation is an unavoidable consequence of the central role of reactive thioesters in metabolism. Finally, we propose a hypothesis for why low-stoichiometry protein acylation is selected against by evolution and how it might contribute to degenerative processes such as aging.

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Section: Low Stoichiometry Protein Acylation Is a Stress With Detrimementioning

confidence: 91%

The Causes and Consequences of Nonenzymatic Protein Acylation

James

Smith

et al. 2018

Trends in Biochemical Sciences

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“…Aging postulates that senescence is related to somatic maintenance (Lemaître et al 2015, Kirkwood 77 2017, one may expect that species who invest more into this item of expenditure such as "slow" 78 species, (i.e., low recruitment and high adult survival), (see Ma & Gladyshev 2017) for the diversity of senescence patterns, suggesting that other mechanisms may be at work as well. 86…”

Section: / 22mentioning

confidence: 99%

Slow life-history strategies are associated with negligible actuarial senescence in western Palearctic salamanders

Cayuela¹,

Olgun

Angelini

et al. 2019

Preprint

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28Actuarial senescence (hereafter "senescence") has been viewed for a long time as an inevitable and 29 uniform process. However, the work on senescence has mainly focused on endotherms (especially 30 mammals) with deterministic growth and low regeneration capacity at adult stages, leading to a 31 strong taxonomic bias in the study of aging. Recent studies have highlighted that senescence could 32 indeed display highly variable trajectory shape that correlates with species life history traits. Slow 33 life histories and indeterminate growth seem to be associated with weak and late senescence. 34Furthermore, a few studies have suggested that high regenerative abilities could make senescence 35 negligible in several ectotherms (e.g., hydra and salamanders). However, demographic data for 36 species that would allow testing of these hypotheses are scarce and fragmented. Here, we 37 investigated senescence patterns in a group of salamanders (i.e. "true salamanders") from the 38 Western Palearctic using capture-recapture data and Bayesian modeling. Our results showed that 39 salamanders have slow life histories and that they experience negligible senescence. This pattern 40 was consistent at both intra-and interspecific levels, suggesting that the absence of senescence may 41 be a phylogenetically conserved trait. The regenerative capacities of true salamanders, and urodeles 42 in general, likely explains why these small ectotherms have lifespans similar to that of large 43 endotherms (e.g., ungulates, large birds) and undergo negligible senescence contrary to most 44 amniotes including humans. Our study seriously challenges the idea that senescence is a ubiquitous 45 phenomenon in the living world. 46 47

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“…Subsequent studies have also demonstrated that intermittent fasting prologs life-span in mice (76). The survival benefit of caloric restriction appears to be related to an effect on aging mechanisms (42, 121). Similarly, caloric restriction was found to improve Doppler parameters of diastolic function in B6D2-F1 hybrid mice, a mouse model of senescent diastolic dysfunction, without an impact on systolic parameters (216).…”

Section: Effects Of Caloric Restriction On Cardiac Physiologymentioning

confidence: 99%

Lysosomes Mediate Benefits of Intermittent Fasting in Cardiometabolic Disease: The Janitor Is the Undercover Boss

Mani

Javaheri

Diwan

2018

Comprehensive Physiology

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Adaptive responses that counter starvation have evolved over millennia to permit organismal survival, including changes at the level of individual organelles, cells, tissues, and organ systems. In the past century, a shift has occurred away from disease caused by insufficient nutrient supply toward overnutrition, leading to obesity and diabetes, atherosclerosis, and cardiometabolic disease. The burden of these diseases has spurred interest in fasting strategies that harness physiological responses to starvation, thus limiting tissue injury during metabolic stress. Insights gained from animal and human studies suggest that intermittent fasting and chronic caloric restriction extend lifespan, decrease risk factors for cardiometabolic and inflammatory disease, limit tissue injury during myocardial stress, and activate a cardioprotective metabolic program. Acute fasting activates autophagy, an intricately orchestrated lysosomal degradative process that sequesters cellular constituents for degradation, and is critical for cardiac homeostasis during fasting. Lysosomes are dynamic cellular organelles that function as incinerators to permit autophagy, as well as degradation of extracellular material internalized by endocytosis, macropinocytosis, and phagocytosis. The last decade has witnessed an explosion of knowledge that has shaped our understanding of lysosomes as central regulators of cellular metabolism and the fasting response. Intriguingly, lysosomes also store nutrients for release during starvation; and function as a nutrient sensing organelle to couple activation of mammalian target of rapamycin to nutrient availability. This article reviews the evidence for how the lysosome, in the guise of a janitor, may be the "undercover boss" directing cellular processes for beneficial effects of intermittent fasting and restoring homeostasis during feast and famine. © 2018 American Physiological Society. Compr Physiol 8:1639-1667, 2018.

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Molecular signatures of longevity: Insights from cross-species comparative studies

Cited by 90 publications

References 111 publications

The Causes and Consequences of Nonenzymatic Protein Acylation

The Causes and Consequences of Nonenzymatic Protein Acylation

Slow life-history strategies are associated with negligible actuarial senescence in western Palearctic salamanders

Lysosomes Mediate Benefits of Intermittent Fasting in Cardiometabolic Disease: The Janitor Is the Undercover Boss

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