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Review
. 2022 Mar 16;11(6):1010.
doi: 10.3390/cells11061010.

Cardiovascular Inflammaging: Mechanisms and Translational Aspects

Affiliations
Review

Cardiovascular Inflammaging: Mechanisms and Translational Aspects

Maria Luisa Barcena et al. Cells. .

Abstract

Aging is one of the major non-reversible risk factors for several chronic diseases, including cancer, type 2 diabetes, dementia, and cardiovascular diseases (CVD), and it is a key cause of multimorbidity, disability, and frailty (decreased physical activity, fatigue, and weight loss). The underlying cellular mechanisms are complex and consist of multifactorial processes, such as telomere shortening, chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, accumulation of senescent cells, and reduced autophagy. In this review, we focused on the molecular mechanisms and translational aspects of cardiovascular aging-related inflammation, i.e., inflammaging.

Keywords: cardiac inflammaging; microbiome; mitochondrial homeostasis; vascular senescence.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of some signaling pathways involved in cardiac inflammaging development and potential treatment strategies. Systemic aging leads to low-grade systemic inflammation, which among numerous other mechanisms includes type 2 diabetes and gut microbiome dysbiosis. Cardiac aging is linked with (i) increased expression of pro-inflammatory factors and immune cell infiltration, (ii) downregulation of main energy regulating mechanisms, such as pAMPK and sirtuin, and (iii) mitochondrial dysfunction. Together with the low-grade systemic inflammation, it leads to cardiac inflammation and endothelial/myocardial dysfunction. The potential treatment strategies are shown.

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