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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

Asporin regulated by miR-26b-5p mediates chondrocyte senescence and exacerbates osteoarthritis progression via TGF-β1/Smad2 pathway.

TL;DR: In this paper, the role and mechanism of asporin in modulating chondrocyte senescence in osteoarthritis (OA) pathology was investigated in mice.
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The emerging role of cellular senescence in complications of COVID-19.

TL;DR: In this paper, the impact of cellular senescence on COVID-19 complications was investigated and potential therapeutic targets for eliminating senescent cells during the CoVirus disease 2019 pandemic were explored.
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Retrotransposons as a Source of DNA Damage in Neurodegeneration

TL;DR: The potential contribution of LINE-1 elements in inducing DNA damage and genomic instability, which are emerging pathological features in NDs, are discussed.
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Cellular senescence and acute kidney injury

TL;DR: In this paper , a review integrates the existing studies on senescence in AKI from several aspects to find meaningful research directions to improve the prognosis of AKI and prevent the progression of CKD.
Journal ArticleDOI

Pulsed electromagnetic fields attenuate glucocorticoid-induced bone loss by targeting senescent LepR+ bone marrow mesenchymal stromal cells

TL;DR: In4a with LepR in longitudinal femoral sections as mentioned in this paper showed that PEMFs alleviate bone loss induced by glucocorticoids by eliminating senescent cells, maintaining angiogenesis-osteogenesis coupling, and shedding light on the mechanisms.
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.
Journal ArticleDOI

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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