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LINE1 Derepression in Aged Wild-Type and SIRT6-Deficient Mice Drives Inflammation

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TLDR
It is reported that SIRT6-deficient cells and tissues accumulate abundant cytoplasmic L1 cDNA, which triggers strong type I interferon response via activation of cGAS, and modulating L1 activity may be an important strategy for attenuating age-related pathologies.
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This article is published in Cell Metabolism.The article was published on 2019-04-02 and is currently open access. It has received 243 citations till now. The article focuses on the topics: Wild type & Interferon.

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Cellular senescence in ageing: from mechanisms to therapeutic opportunities

TL;DR: The mechanisms and modulators of cellularsenescence establishment and induction of a senescence-associated secretory phenotype are discussed, and the potential of senolytic and senomorphic therapies in ageing and associated diseases is provided.
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The cGAS-STING pathway as a therapeutic target in inflammatory diseases.

TL;DR: The cGAS-STING pathway has emerged as a key mediator of inflammation in the settings of infection, cellular stress and tissue damage as discussed by the authors, which has enabled the development of selective small-molecule inhibitors with the potential to target the CGS-STing axis in a number of inflammatory diseases.
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The ageing epigenome and its rejuvenation.

TL;DR: The epigenetic changes that occur during ageing and the rapidly increasing knowledge of how these epigenetic mechanisms have an effect on healthspan and lifespan extension are discussed, and questions to guide future research on interventions to rejuvenate the epigenome and delay ageing processes are outlined.
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Hallmarks of aging: An expanding universe

TL;DR: In this paper , the authors proposed the following hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis.
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The quest to slow ageing through drug discovery

TL;DR: The most promising interventions to slow ageing are examined and group them into two tiers based on the robustness of the preclinical, and some clinical, results, in which the top tier includes rapamycin, senolytics, metformin, acarbose, spermidine, NAD + enhancers and lithium.
References
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Journal ArticleDOI

Initial sequencing and analysis of the human genome.

Eric S. Lander, +248 more
- 15 Feb 2001 - 
TL;DR: The results of an international collaboration to produce and make freely available a draft sequence of the human genome are reported and an initial analysis is presented, describing some of the insights that can be gleaned from the sequence.
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The Hallmarks of Aging

TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
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Initial sequencing and comparative analysis of the mouse genome.

Robert H. Waterston, +222 more
- 05 Dec 2002 - 
TL;DR: The results of an international collaboration to produce a high-quality draft sequence of the mouse genome are reported and an initial comparative analysis of the Mouse and human genomes is presented, describing some of the insights that can be gleaned from the two sequences.
Journal ArticleDOI

Type I interferons in infectious disease.

TL;DR: Experimental models of tuberculosis have demonstrated that prostaglandin E2 and interleukin-1 inhibit type I IFN expression and its downstream effects, demonstrating that a cross-regulatory network of cytokines operates during infectious diseases to provide protection with minimum damage to the host.
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Initial sequencing and analysis of the human genome.

Eric S. Lander, +248 more
- 15 Feb 2001 -