Abstract
Age-associated changes leading to a decline in cardiac structure and function contribute to the increased susceptibility and incidence of cardiovascular diseases (CVD) in elderly individuals. Indeed, age is considered a risk factor for heart failure and serves as an important predictor for poor prognosis in elderly individuals. Effects stemming from chronic, low-grade inflammation, inflammaging, are considered important determinants in cardiac health; however, our understanding of the mechanisms involved remains unresolved. A steady decline in mitochondrial function is recognized as an important biological consequence found in the aging heart which contributes to the development of heart failure. Dysfunctional mitochondria contribute to increased cellular stress and an innate immune response by activating the NLRP-3 inflammasomes, which have a role in inflammaging and age-related CVD pathogenesis. Emerging evidence suggests a protective role for CYP450 epoxygenase metabolites of N-3 and N-6 polyunsaturated fatty acids (PUFA), epoxylipids, which modulate various aspects of the immune system and protect mitochondria. In this article, we provide insight into the potential roles N-3 and N-6 PUFA have modulating mitochondria, inflammaging and heart failure.
Highlights
Aging is a key determinant of cardiovascular health, as evidenced from an exponential increase in the prevalence of cardiovascular disease (CVD) in the geriatric population [1]
Clinical and epidemiological studies reported that the cardioprotective effects of the epoxylipids derived from N-3 and N-6 polyunsaturated fatty acids (PUFA) against various cardiac pathologies are attributed to their immunomodulatory properties
EETs ameliorated inflammatory responses in human endothelial cells subjected to TNF-α-stimulated inflammation, by decreasing the expression of cytokine-induced adhesion molecule, vascular cell adhesion molecule–1 (VCAM-1) and preventing leucocyte adhesion attributed to inhibition of nuclear transcription factor-kappa B (NF-kB) activity
Summary
Aging is a key determinant of cardiovascular health, as evidenced from an exponential increase in the prevalence of cardiovascular disease (CVD) in the geriatric population [1]. There are several age-related alterations in cardiovascular function and structure, such as atrial stiffening, vascular fibrosis and thickening, LV hypertrophy, and insufficient mitochondrial energy production. These distinctive changes may partly explain why elderly individuals are more likely to develop HFpEF [23,24]. Chronic inflammation is a key component of aging and aging-related pathologies associated with increased risk of cardiovascular morbidity and mortality [35]. Studies in experimental animal models and human hearts suggest that mitochondria play a central role in the aging process and abnormalities in mitochondrial function and structure are considered major drivers of age-associated cardiac dysfunction [3,40,41]. Enhancing our understanding of inflammatory pathways interwoven with mitochondrial events in the process of cardiac aging remains important, notably toward developing more promising therapeutics for age-associated pathologies, including HF
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