scispace - formally typeset
Open AccessJournal ArticleDOI

Source of Chronic Inflammation in Aging.

Reads0
Chats0
TLDR
The factors and cellular pathways/processes that are known to regulate low-grade persistent inflammation in aging and age-related disease are summarized.
Abstract
Aging is a complex process that results from a combination of environmental, genetic, and epigenetic factors. A chronic pro-inflammatory status is a pervasive feature of aging. This chronic low-grade inflammation occurring in the absence of overt infection has been defined as “inflammaging” and represents a significant risk factor for morbidity and mortality in the elderly. The low-grade inflammation persists even after reversing pro-inflammatory stimuli such as LDL cholesterol and the renin–angiotensin system (RAS). Recently, several possible sources of chronic low-grade inflammation observed during aging and age-related diseases have been proposed. Cell senescence and dysregulation of innate immunity is one such mechanism by which persistent prolonged inflammation occurs even after the initial stimulus has been removed. Additionally, the coagulation factor that activates inflammatory signaling beyond its role in the coagulation system has been identified. This signal could be a new source of chronic inflammation and cell senescence. Here, we summarized the factors and cellular pathways/processes that are known to regulate low-grade persistent inflammation in aging and age-related disease.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

Why does COVID-19 disproportionately affect older people?

TL;DR: The molecular differences between young, middle-aged and older people that may explain why COVID-19 is a mild illness in some but life-threatening in others are presented and treatments that could increase the survival of older people are discussed.
Journal ArticleDOI

Measuring biological aging in humans: A quest.

TL;DR: Current research focuses on measuring the pace of aging to identify individuals who are “aging faster” to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging.
Journal ArticleDOI

Benefits of Metformin in Attenuating the Hallmarks of Aging

TL;DR: Metformin's mechanisms in attenuating hallmarks of aging and their interconnectivity, by improving nutrient sensing, enhancing autophagy and intercellular communication, protecting against macromolecular damage, delaying stem cell aging, modulating mitochondrial function, regulating transcription, and lowering telomere attrition and senescence, make metformin an attractive gerotherapeutic to translate to human trials.
Journal ArticleDOI

The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging".

TL;DR: The aim of the present review was to summarize experimental data and clinical observations that linked the pathophysiology mechanisms of “inflamm-aging”, mild-grade inflammation, and cytokine storm in some elderly adults with severe COVID-19 infection.
Journal ArticleDOI

The integration of inflammaging in age-related diseases.

TL;DR: The concept of inflammaging is described, being a chronic, systemic, low grade and therefore for a long time subclinical, inflammatory process, and how it is integrated in the context of ARD.
References
More filters
Journal ArticleDOI

Obesity is associated with macrophage accumulation in adipose tissue

TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
Journal ArticleDOI

Circulating mitochondrial DAMPs cause inflammatory responses to injury

TL;DR: It is shown that injury releases mitochondrial DAMPs into the circulation with functionally important immune consequences, including formyl peptides and mitochondrial DNA, which promote PMN Ca2+ flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo.
Journal ArticleDOI

Clearance of p16 Ink4a -positive senescent cells delays ageing-associated disorders

TL;DR: Data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.
Journal ArticleDOI

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.
Related Papers (5)