Abstract
Aging is a major risk factor in the development of chronic diseases affecting various tissues including the cardiovascular system, muscle and bones. Age-related diseases are a consequence of the accumulation of cellular damage and reduced activity of protective stress response pathways leading to low-grade systemic inflammation and oxidative stress. Both inflammation and oxidative stress are major contributors to cellular senescence, a process in which cells stop proliferating and become dysfunctional by secreting inflammatory molecules, reactive oxygen species (ROS) and extracellular matrix components that cause inflammation and senescence in the surrounding tissue. This process is known as the senescence associated secretory phenotype (SASP). Thus, accumulation of senescent cells over time promotes the development of age-related diseases, in part through the SASP. Polyphenols, rich in fruits and vegetables, possess antioxidant and anti-inflammatory activities associated with protective effects against major chronic diseases, such as cardiovascular disease (CVD). In this review, we discuss molecular mechanisms by which polyphenols improve anti-oxidant capacity, mitochondrial function and autophagy, while reducing oxidative stress, inflammation and cellular senescence in vascular smooth muscle cells (VSMCs) and endothelial cells (ECs). We also discuss the therapeutic potential of polyphenols in reducing the effects of the SASP and the incidence of CVD.
Highlights
Normal cell metabolism results in the generation of damaging free radicals, including reactive oxygen species (ROS) that are eliminated by antioxidant enzymes
The purpose of this review is to evaluate the most current research testing the role of foods rich in polyphenols and specific phenolic compounds in pathways upregulated during aging
We demonstrated that activation of nuclear factor-κB (NF-κB) by zinc overload was mediated by mitochondrial ROS since the mitochondrial ROS scavenger MitoTEMPO (Mitochondria-targeted (2,2,6,6-tetramethylpiperidin-1yl) oxyl) reduced NF-κB activation, NADPH oxidase 1 (Nox1) expression and senescence [16]
Summary
Normal cell metabolism results in the generation of damaging free radicals, including reactive oxygen species (ROS) that are eliminated by antioxidant enzymes. Overtime, increased expression of ROS-generating molecules and/or reduced expression of antioxidant enzymes, like catalase, superoxide dismutases (SODs), and glutathione peroxidases (GPxs) promote the accumulation of ROS leading to damage to DNA, lipids and proteins. Accumulation of damaged molecules and downregulation of mitochondrial function, which causes oxidative stress, are associated with aging and increased incidence of age-related diseases, including cardiovascular disease (CVD), cancer, and other chronic disease states. Recently has aging itself been viewed as a treatable condition, with an etiology related to excessive ROS levels that lead to cellular senescence, a process by which cells enter a permanent state of cell cycle arrest. An additional aim is to discuss possible mechanisms by which polyphenols exert their biological effects in senescence pathways
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