Atherosclerosis is an autoimmune disease caused by self- and non-self-antigens contributing to excessive activation of T and B cell immune responses. These responses further aggravate vascular infiammation and promote progression of atherosclerosis and vulnerability to plaques via releasing pro-infiammatory cytokines. Regulatory T cells (Tregs) as the major immunoregulatory cells, in particular, induce and maintain immune homeostasis and tolerance by suppressing the immune responses of various cells such as T and B cells, natural killer (NK) cells, monocytes, and dendritic cells (DCs), as well as by secreting inhibitory cytokines interleukin (IL)-10, IL-35 and transcription growth factor β (TGF-β) in both physiological and pathological states. Numerous evidence demonstrates that reduced numbers and dysfunction of Treg may be involveved in atherosclerosis pathogenesis. Increasing or restoring the numbers and improving the immunosuppressive capacity of Tregs may serve as a fundamental immunotherapy to treat atherosclerotic cardiovascular diseases. In this article, we briefiy present current knowledge of Treg subsets, summarize the relationship between Tregs and atherosclerosis development, and discuss the possibilities of regulating Tregs for prevention of atherosclerosis pathogenesis and enhancement of plaque stability. Although the exact molecular mechanisms of Treg-mediated protection against atherosclerosis remain to be elucidated, the strategies for targeting the regulation of Tregs may provide specific and significant approaches for the prevention and treatment of atherosclerotic cardiovascular diseases.

Atherosclerosis is characterized by the accumulation of lipids and deposition of fibrous elements in the vascular wall, which is the primary cause of cardiovascular diseases. Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor of energy metabolism that regulates multiple physiological processes, including lipid and glucose metabolism and the normalization of energy imbalances. Overwhelming evidence indicates that AMPK activation markedly attenuates atherosclerosis development. Autophagy inhibits cell apoptosis and inflammation and promotes cholesterol efflux and efferocytosis. Physiological autophagy is essential for maintaining normal cardiovascular function. Increasing evidence demonstrates that autophagy occurs in developing atherosclerotic plaques. Emerging evidence indicates that AMPK regulates autophagy via a downstream signaling pathway. The complex relationship between AMPK and autophagy has attracted the attention of many researchers because of this close relationship to atherosclerosis development. This review demonstrates the role of AMPK and autophagy in atherosclerosis. An improved understanding of this interrelationship will create novel preventive and therapeutic strategies for atherosclerosis.

No abstract

Advanced oxidation protein products (AOPPs) are novel biomarkers of oxidative damage to proteins and a novel class of inflammatory mediators. AOPPs can promote oxidative stress (OS) and inflammation and thus participate in many pathophysiological disease processes. Atherosclerosis is a chronic inflammatory disease of blood vessels that is characterized by low-density lipoprotein infiltration into the endothelial intima and the formation of atherosclerotic plaques. Inflammation and OS are established risk factors for the formation of atherosclerosis. Accumulated studies show that AOPPs can accelerate the progression of atherosclerosis through OS and inflammation. Additionally, AOPPs can accelerate the formation of atherosclerotic plaques by inhibiting high-density lipoprotein receptor scavenger receptor class B type I-mediated high-density lipoprotein cholesterol reverse transport, leading to metabolic disturbances. Some studies have suggested that plasma AOPPs levels are independently positively correlated with blood pressure and are also independent risk factors for cardiovascular disease. AOPPs can trigger oxidative bursts of neutrophils, monocytes and phagocytic cells, increase the generation of reactive oxygen species and promote the secretion of cytokines to accelerate endothelial cell injury. Detecting the levels and inhibiting the formation of AOPPs may provide a novel approach to monitor the progress and improve the prognosis of atherosclerosis.

No abstract