Overview: the modulation of ageing through altered proteostasis

Miller, Benjamin F.; Hamilton, Karyn L.

doi:10.1113/jp274997

Cited by 3 publications

(1 citation statement)

References 12 publications

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“…The increased functional demand leads to metabolic and physical stress, and production of excessive heat and free radicals, which may accelerate the cell entropy [27]. The excess capacity of bioenergetics pathway intermediates affects the aging process through altering the cell epigenetic patterns as documented by the increased levels of acetyl-CoA and NAD in aging Drosophila and mice, seem to influence the lifespan by altering the epigenetics balance [28,29]. The glycolytic pathway as such has excess capacity in vivo and its excess metabolic capacity is demonstrated by excess activity its enzymes, such as phosphorglucose isomerase, phosphor-glucomutase, triosephosphate isomerase and glycerol-phosphate dehydrogenase, which are present in considerable excess capacity.…”

Section: Excess Metabolic Capacity Of Bioenergetics Pathwaysmentioning

confidence: 99%

The Concepts of Biorhythms, Redundancy and Reserve: Impact on Cardiovascular Aging and Disease

Nikhra

2019

OAJGGM

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Biorhythms, redundancy and reserve:The dynamic equilibrium in the interactions of biorhythms with the rhythms of the surrounding ecosystem forms the basis of life. The biorhythms can be categorized by their relationship to 24-h day cycle as circadian, ultradian and infradian. In addition, there are other rhythmic patterns generated outside the CNS, such as the cardiac rhythm. In addition, there are rhythmic contractions of muscles controlling gastrointestinal motility and uterine contractions. The organ reserve is the ability of an organ to endure recurring stressful conditions and restore the homeostasis and normal physiological function. There occurs age-related decline in physiological functions attributable to loss of organ reserve due to multiple factors. Molecular basis of reserve and redundancy:The intermediary metabolism comprising of cellular biochemical reactions and metabolites is enriched with biochemical steps or intracellular structures exhibiting excess metabolic capacity than required for normal basic functions. In addition, the mitochondrial DNA (mtDNA) found in multi-copies, serves as a structural excess capacity for cellular energy metabolism. Similarly, the DNA repeats in telomeres serve as structural excess capacity for repair. The organ reserve is, thus, a joint contribution of excess metabolic capacities of several metabolic pathways and biochemical structures enabling a built-in robust metabolism and structural mechanisms for stress response and repair. Physiology of metabolic reserve and redundancy:The living systems owe their survival to a series of complex biochemical pathways for maintenance and repair, and the defence systems creating the homeo-dynamic space which provides the buffering capacity for a biological system. The aging and the age-related diseases can be held as the consequences of a progressive shrinkage of the homeo-dynamic space, due to failure of maintenance and repair. The senescent changes occur in the cells, tissues and organs, and in turn affect the functioning of the biological systems. At subcellular level, mitochondrial oxidative stress and dysfunction play an important role in aging, and microRNAs (miRNAs) are important regulators of aging and age-related diseases. Impact of senescence of organs and systems:Various stimuli appear to converge on certain pathways that influence cell cycle regulation, DNA repair and apoptosis, and the process of cellular senescence. At the cellular level, these pathways are regulated by the tumor suppressor proteins p53 and pRb. The p53 is a crucial mediator of the cellular response to damaged DNA and dysfunctional telomeres, and in turn activates the cyclin-dependent inhibitor p21. The senescence is induced at cellular level via the p53 pathway in response to DNA damage and telomere dysfunction, whereas the p16/pRb pathway mediates senescence caused by oncogenic stimuli, chromatin disruption, and other cellular stresses. The aging of organs is progressive and irreversible, and associated with increased incidence and prevalence of ...

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Section: Excess Metabolic Capacity Of Bioenergetics Pathwaysmentioning

confidence: 99%

The Concepts of Biorhythms, Redundancy and Reserve: Impact on Cardiovascular Aging and Disease

Nikhra

2019

OAJGGM

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Is Impaired Proteodynamics a Key to Understand the Biomarkers of Human Cellular Aging?

Witkowski

Bryl

Fülöp

2019

Healthy Ageing and Longevity

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Implications of Long Non-Coding RNAs in Age-Altered Proteostasis

Cătană¹,

Crişan²,

Opre³

et al. 2020

Aging and disease

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This review aims to summarize the current knowledge on how lncRNAs are influencing aging and cancer metabolism. Recent research has shown that senescent cells re-enter cell-cycle depending on intrinsic or extrinsic factors, thus restoring tissue homeostasis in response to age-related diseases (ARDs). Furthermore, maintaining proteostasis or cellular protein homeostasis requires a correct quality control (QC) of protein synthesis, folding, conformational stability, and degradation. Long non-coding RNAs (lncRNAs), transcripts longer than 200 nucleotides, regulate gene expression through RNA-binding protein (RBP) interaction. Their association is linked to aging, an event of proteostasis collapse. The current review examines approaches that lead to recognition of senescence-associated lncRNAs, current methodologies, potential challenges that arise from studying these molecules, and their crucial implications in clinical practice.

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Overview: the modulation of ageing through altered proteostasis

Cited by 3 publications

References 12 publications

The Concepts of Biorhythms, Redundancy and Reserve: Impact on Cardiovascular Aging and Disease

The Concepts of Biorhythms, Redundancy and Reserve: Impact on Cardiovascular Aging and Disease

Is Impaired Proteodynamics a Key to Understand the Biomarkers of Human Cellular Aging?

Implications of Long Non-Coding RNAs in Age-Altered Proteostasis

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