Abstract
Although many cardiovascular (CVD) medications, such as antithrombotics, statins, and antihypertensives, have been identified to treat atherosclerosis, at most, many of these therapeutic agents only delay its progression. A growing body of evidence suggests physical exercise could be implemented as a non-pharmacologic treatment due to its pro-metabolic, multisystemic, and anti-inflammatory benefits. Specifically, it has been discovered that certain anti-inflammatory peptides, metabolites, and RNA species (collectively termed “exerkines”) are released in response to exercise that could facilitate these benefits and could serve as potential therapeutic targets for atherosclerosis. However, much of the relationship between exercise and these exerkines remains unanswered, and there are several challenges in the discovery and validation of these exerkines. This review primarily highlights major anti-inflammatory exerkines that could serve as potential therapeutic targets for atherosclerosis. To provide some context and comparison for the therapeutic potential of exerkines, the anti-inflammatory, multisystemic benefits of exercise, the basic mechanisms of atherosclerosis, and the limited efficacies of current anti-inflammatory therapeutics for atherosclerosis are briefly summarized. Finally, key challenges and future directions for exploiting these exerkines in the treatment of atherosclerosis are discussed.
Highlights
Atherosclerosis and its clinical manifestations in coronary heart disease, stroke, and peripheral artery disease are the leading cause of morbidity and mortality in the Western world [1]
high-density lipoprotein (HDL) from these patient populations has been found to have no protective vascular effects or could even cause paradoxical harmful effects [34]. This may be caused by significant changes in their pathological structure in an acute-phase reaction, during which HDL is characterized by increased concentrations of serum amyloid A, type 2 secretory phospholipase A2, and ceruloplasmin, and lower concentrations of apolipoprotein A1 [33]
As physical exercise brings about a reduction in visceral fat and increases energy expenditure, it subsequently results in lower production of pro-inflammatory adipokines, including tumor necrosis factor (TNF), leptin, retinol-binding protein 4, lipocalin 2, interleukin-6 (IL-6), interleukin-18 (IL-18), CC-chemokine ligand 2 (CCL2 or monocyte chemoattractant protein 1 (MCP-1)), CXC-chemokine ligand 5, and angiopoietin-like protein 2 and an increase in anti-inflammatory cytokines, such as adiponectin and secreted frizzled-related protein 5 [9,59]
Summary
Atherosclerosis and its clinical manifestations in coronary heart disease, stroke, and peripheral artery disease are the leading cause of morbidity and mortality in the Western world [1]. Due to its pro-metabolic, multisystemic, and anti-inflammatory benefits, physical exercise has been prescribed as a non-pharmacologic treatment for atherosclerosis, as it boosts high-density lipoprotein (HDL) levels while lowering LDL levels, and reduces the risk of many chronic diseases, including type 2 diabetes and cancer. It has a number of anti-inflammatory effects, including reducing visceral fat, increasing levels of nitric oxide (NO), and secreting anti-inflammatory exerkines from skeletal muscles and other secretory organs. Understanding the role of exercise and exerkines in the prevention of atherosclerosis may lead to future development of bioengineered targets in the treatment of atherosclerosis
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