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Chronic Inflammation: Accelerator of Biological Aging.

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TLDR
This review will cover the identification of pathways that control age-related inflammation across multiple systems and its potential causal role in contributing to adverse health outcomes.
Abstract
Biological aging is characterized by a chronic low-grade inflammation level. This chronic phenomenon has been named "inflamm-aging" and is a highly significant risk factor for morbidity and mortality in the older persons. The most common theories of inflamm-aging include redox stress, mitochondrial dysfunction, glycation, deregulation of the immune system, hormonal changes, epigenetic modifications, and dysfunction telomere attrition. Inflamm-aging plays a role in the initiation and progression of age-related diseases such as type II diabetes, Alzheimer's disease, cardiovascular disease, frailty, sarcopenia, osteoporosis, and cancer. This review will cover the identification of pathways that control age-related inflammation across multiple systems and its potential causal role in contributing to adverse health outcomes.

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Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor

TL;DR: Coppe et al. as mentioned in this paper showed that human cells induced to senesce by genotoxic stress secrete myriad factors associated with inflammation and malignancy, including interleukin (IL)-6 and IL-8.
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Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

TL;DR: A better understanding of the role of antioxidants involved in redox modulation of inflammation would provide a useful approach for potential interventions, and subsequently promoting healthy longevity.
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Fighting against Skin Aging: The Way from Bench to Bedside.

TL;DR: This review summarizes changes in skin aging, research advances of the molecular mechanisms leading to these changes, and the treatment strategies aimed at preventing or reversing skin aging.
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Redefining Chronic Inflammation in Aging and Age-Related Diseases: Proposal of the Senoinflammation Concept.

TL;DR: This review discusses newly emerging data on multi-phase inflammatory networks and proinflammatory pathways as they relate to aging and provides a schema highlighting the important and ever-increasing roles of proinflammatory senescence-associated secretome, inflammasome, ER stress, TLRs, and microRNAs, which support the senoinflammation concept.
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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
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Inflammation and cancer

TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
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Acute-Phase Proteins and Other Systemic Responses to Inflammation

TL;DR: A large number of changes, distant from the site or sites of inflammation and involving many organ systems, may accompany inflammation, and the mechanisms mediating them are becoming better understood.
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Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men

TL;DR: The reduction associated with the use of aspirin in the risk of a first myocardial infarction appears to be directly related to the level of C-reactive protein, raising the possibility that antiinflammatory agents may have clinical benefits in preventing cardiovascular disease.
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Adipose Tissue as an Endocrine Organ

TL;DR: An overview of the endocrine functions of adipose tissue can be found in this paper, where the authors highlight the adverse metabolic consequences of both adipose excess and deficiency, and propose a more rational therapy for these increasingly prevalent disorders.
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Inflamm‐aging: An Evolutionary Perspective on Immunosenescence

TL;DR: The beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
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