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Senescent cells: an emerging target for diseases of ageing.

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TLDR
Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.
Abstract
Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.

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Journal ArticleDOI

Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process.

TL;DR: This review aims to address the latest information about the different mechanisms related to neuroplasticity and neuronal death and to provide strategies that can improve neuroprotection and decrease the neurodegeneration caused by aging and environmental stressors.
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Cellular senescence in musculoskeletal homeostasis, diseases, and regeneration

TL;DR: In this article, the role of senescent cells in the maintenance of bone homeostasis during childhood and their contribution to the pathogenesis of chronic musculoskeletal disorders, including osteoporosis, osteoarthritis, and sarcopenia.
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The mitomiR/Bcl-2 axis affects mitochondrial function and autophagic vacuole formation in senescent endothelial cells

TL;DR: It is documented for the first time that some mitomiRs can act as mediators of the multiple but functionally linked biochemical and morphological changes that characterize aging cells and that they can promote different cellular outcomes according to the senescence status of the cell.
Journal ArticleDOI

Recent advances in the field of caloric restriction mimetics and anti-aging molecules.

TL;DR: Novel CR mimetics and anti-aging compounds, such as alpha-ketoglutarate, 4,4'-dimethoxychalcone, fungal polysaccharides, inorganic nitrate, and trientine are reviewed, highlighting their possible molecular targets and mechanisms of action.
Journal ArticleDOI

Targeting p16-induced senescence prevents cigarette smoke-induced emphysema by promoting IGF1/Akt1 signaling in mice

TL;DR: It is suggested that targeting senescence pathways may facilitate alveolar regeneration in chronic obstructive pulmonary diseases by activating cell-proliferation signals through insulin-like growth factor 1.
References
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Journal ArticleDOI

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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A biomarker that identifies senescent human cells in culture and in aging skin in vivo

TL;DR: It is shown that several human cells express a beta-galactosidase, histochemically detectable at pH 6, upon senescence in culture, which provides in situ evidence that senescent cells may exist and accumulate with age in vivo.
Journal ArticleDOI

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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