Unveiling the Role of Inflammation and Oxidative Stress on Age-Related Cardiovascular Diseases

Abstract

The global population above 60 years has been growing exponentially in the last decades, which is accompanied by an increase in the prevalence of age-related chronic diseases, highlighting cardiovascular diseases (CVDs), such as hypertension, atherosclerosis, and heart failure. Aging is the main risk factor for these diseases. Such susceptibility to disease is explained, at least in part, by the increase of oxidative stress, in which it damages cellular components such as proteins, DNA, and lipids. In addition, the chronic inflammatory process in aging “inflammaging” also contributes to cell damage, creating a stressful environment which drives to the development of CVDs. Taken together, it is possible to identify the molecular connection between oxidative stress and the inflammatory process, especially by the crosstalk between the transcription factors Nrf-2 and NF-κB which are mediated by redox signalling and are involved in aging. Therapies that control this process are key targets in the prevention/combat of age-related CVDs. In this review, we show the basics of inflammation and oxidative stress, including the crosstalk between them, and the implications on age-related CVDs.

Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities

“…Conversely, the rising leptin levels in the heart positively correlate with coronary artery disease, left ventricular hypertrophy, stroke, and myocardial infarction ( Soderberg et al., 1999 ; Wallace et al., 2001 ; Chait and den Hartigh, 2020 ). Along with pro-inflammatory circulating signals, a transcription factor, NF- κ B, is a product of chronic inflammation in cardiovascular tissue and is a useful clinical indicator for obesity-related inflammation ( de Almeida et al., 2020 ).…”

Nrf2 Alleviates TNF-α-Induced Oxidative Stress Damage in Type II Alveolar Epithelial Cells by Down-Regulating the Expression of NOX1

“…More importantly, NF-κB also possesses the ability to regulate the expression activity of NOX1, via binding its element in the promoter of NOX1 [27] and it is mainly activated by TNF-α [28] . Additionally, increasing evidence indicated that there is a crosstalk between Nrf2 and NF-κB [29,30] . Thus, NF-κB might participate in the downregulation of Nrf2 on the expression of NOX1 and the level of oxidative stress in T 2 AECs induced by TNF-α.…”

The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress in cardiovascular diseases

“…The chronic low-grade, systemic and local inflammation that develops during obesity links obesity to the development of insulin resistance (Gregor and Hotamisligil 2011 ), which then effects a variety of different organs involved in the control of metabolic homeostasis, including adipose tissue, liver, endocrine pancreas, hypothalamus, and possibly skeletal muscle. As adipocytes are a known source of pro-inflammatory cytokines, including TNF-α, IL-1, and IL-6, obesity can be seen as a chronic inflammatory condition (de Almeida et al 2020 ; Franssen et al 2016 ; Schmidt-Lucke et al 2015 ). These cytokines are known potent stimulators of the production of ROS and NOS by macrophages and monocytes and thereby increasing oxidative stress.…”