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Review
. 2022 May 18:10:882211.
doi: 10.3389/fcell.2022.882211. eCollection 2022.

Modern Concepts in Cardiovascular Disease: Inflamm-Aging

Yustina M Puspitasari  1 , Stefano Ministrini  1   2 , Lena Schwarz  1 , Caroline Karch  1 , Luca Liberale  1   3   4 , Giovanni G Camici  1   5   6
Affiliations
Review

Modern Concepts in Cardiovascular Disease: Inflamm-Aging

Yustina M Puspitasari et al. Front Cell Dev Biol. .

Abstract

The improvements in healthcare services and quality of life result in a longer life expectancy and a higher number of aged individuals, who are inevitably affected by age-associated cardiovascular (CV) diseases. This challenging demographic shift calls for a greater effort to unravel the molecular mechanisms underlying age-related CV diseases to identify new therapeutic targets to cope with the ongoing aging "pandemic". Essential for protection against external pathogens and intrinsic degenerative processes, the inflammatory response becomes dysregulated with aging, leading to a persistent state of low-grade inflammation known as inflamm-aging. Of interest, inflammation has been recently recognized as a key factor in the pathogenesis of CV diseases, suggesting inflamm-aging as a possible driver of age-related CV afflictions and a plausible therapeutic target in this context. This review discusses the molecular pathways underlying inflamm-aging and their involvement in CV disease. Moreover, the potential of several anti-inflammatory approaches in this context is also reviewed.

Keywords: aging; cardiovascular disease; inflammaging; inflammation; senescence.

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Conflict of interest statement

LL and GGC are coinventors on the International Patent (WO/2020/226993) filed in April 2020 and relating to the use of antibodies which specifically bind IL-1α to reduce various sequelae of ischemia-reperfusion injury to the central nervous system. GGC is a consultant to Sovida solutions limited. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Multifactorial mechanisms of inflamm-aging. Several molecular pathways are involved in triggering age-related chronic low-grade inflammation. Aging affects both innate and adaptive immune systems, leading to sustained low-grade immune activation and reduced sensitivity to appropriate immunogenic stimuli. Such deterioration contributes to inadequate senescent cell clearance. Consequently, the accumulation of senescent cells induces chronic exposure to inflammatory SASP proteins. Aberrant inflammasome activation also occurs in aging due to defects in autophagy and mitophagy, thus further perpetuating the age-related pro-inflammatory milieu. SASP = senescence-associated secretory phenotype; ROS = Reactive oxygen species; NLRP3 = Nod-like receptor protein 3; ASC = Apoptosis speck-like protein; IL = Interleukin (Created with BioRender.com)
See this image and copyright information in PMC

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