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Redox control of senescence and age-related disease

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TLDR
The known biological theories of aging are reviewed and how ROS mechanistically control senescence and the aging process are described and the redox-regulated signaling networks controlling the SASP and its important role in driving age-related diseases are described.
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Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor

TL;DR: Coppe et al. as mentioned in this paper showed that human cells induced to senesce by genotoxic stress secrete myriad factors associated with inflammation and malignancy, including interleukin (IL)-6 and IL-8.
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Oxidative stress, aging, and diseases.

TL;DR: Given the important role of oxidative stress in the pathogenesis of many clinical conditions and aging, antioxidant therapy could positively affect the natural history of several diseases, but further investigation is needed to evaluate the real efficacy of these therapeutic interventions.
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Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype

TL;DR: In this article, the molecular mechanisms that underlie cellular senescence and the senescent associated growth arrest with a particular focus on why cells stop dividing, the stability of the growth arrest, the hypersecretory phenotype and how the different pathways are all integrated.
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Role of p53 in the Regulation of Cellular Senescence

TL;DR: The p53-mediated regulation of several pathophysiological microenvironments that could be associated with senescence and its development are discussed, including the surrounding tissue microenvironment and the neighboring cells by secreting pro-inflammatory cytokines.
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Hallmarks of senescence and aging.

TL;DR: It is considered that the telomere length is the weak biomarker (with poor predictive accuracy), and there is currently no reliable biomarker that meets all the necessary criteria.
References
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Journal ArticleDOI

Aging: A Theory Based on Free Radical and Radiation Chemistry

TL;DR: It seems possible that one factor in aging may be related to deleterious side attacks of free radicals (which are normally produced in the course of cellular metabolism) on cell constituents.
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The serial cultivation of human diploid cell strains.

TL;DR: A consideration of the cause of the eventual degeneration of these strains leads to the hypothesis that non-cumulative external factors are excluded and that the phenomenon is attributable to intrinsic factors which are expressed as senescence at the cellular level.
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The limited in vitro lifetime of human diploid cell strains

TL;DR: The survival curves obtained with human diploid cell strains are comparable to “multiple-hit” or “ multiple-target” curves obtain with other biological systems where an initial threshold dose is required before an exponential form of the curve is established.
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TOR signaling in growth and metabolism.

TL;DR: The physiological consequences of mammalianTORC1 dysregulation suggest that inhibitors of mammalian TOR may be useful in the treatment of cancer, cardiovascular disease, autoimmunity, and metabolic disorders.
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Telomeres shorten during ageing of human fibroblasts.

TL;DR: The amount and length of telomeric DNA in human fibroblasts does in fact decrease as a function of serial passage during ageing in vitro and possibly in vivo.
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