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Open AccessJournal ArticleDOI

Canonical Nlrp3 Inflammasome Links Systemic Low-Grade Inflammation to Functional Decline in Aging

TLDR
Nlrp3 inflammasome is revealed as an upstream target that controls age-related inflammation and an innovative therapeutic strategy to lower NLRp3 activity to delay multiple age- related chronic diseases is offered.
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Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases

TL;DR: The session on inflammation of the Advances in Gerosciences meeting held at the National Institutes of Health/National Institute on Aging in Bethesda on October 30 and 31, 2013 was aimed at defining these important unanswered questions about inflammaging.
Journal ArticleDOI

Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty

TL;DR: Whether therapies to modulate inflammageing can reduce the age-related decline in health is discussed, and the hypothesis that inflammation affects CVD, multimorbidity, and frailty is supported by mechanistic studies but requires confirmation in humans.
Journal ArticleDOI

Ageing as a risk factor for neurodegenerative disease.

TL;DR: Hallmarks of ageing — genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication — correlate with susceptibility to neurodegenerative disease.
Journal ArticleDOI

The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease

TL;DR: In vivo, BHB or a ketogenic diet attenuates caspase-1 activation and IL-1β secretion in mouse models of NLRP3-mediated diseases such as Muckle–Wells syndrome, familial cold autoinflammatory syndrome and urate crystal–induced peritonitis and the findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be linked to BHB-mediated inhibition of theNLRP3 inflammasome.
References
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Journal ArticleDOI

Evolution of Inflammatory Diseases

TL;DR: The inflammatory response is examined from an evolutionary perspective and unique aspects of the inflammatory response and its evolutionary history can help explain the association between inflammation and modern human diseases.
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High-Fat Diet Triggers Inflammation-Induced Cleavage of SIRT1 in Adipose Tissue To Promote Metabolic Dysfunction

TL;DR: It is shown that high-fat diet induces the cleavage of SIRT1 protein in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction.
Journal ArticleDOI

T cell development and receptor diversity during aging.

TL;DR: Emerging data suggest that the end of the 7th decade of life defines a critical time period when T cell homeostasis is no longer guaranteed and diversity of the naïve T-cell repertoire collapses.
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Aging is associated with an increase in T cells and inflammatory macrophages in visceral adipose tissue

TL;DR: A unique inflammatory cell signature in the physiologic context of aging adipose tissue that differs from those induced in setting of diet-induced obesity is demonstrated.
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