Abstract
Cardiovascular disease (CVD) is responsible for 31% of all global deaths. Atherosclerosis is the major cause of cardiovascular disease and is a chronic inflammatory disorder in the arteries. Atherosclerosis is characterized by the accumulation of cholesterol, extracellular matrix, and immune cells in the vascular wall. Recently, the collectin surfactant protein-D (SP-D), an important regulator of the pulmonary immune response, was found to be expressed in the vasculature. Several in vitro studies have examined the role of SP-D in the vascular inflammation leading to atherosclerosis. These studies show that SP-D plays a dual role in the development of atherosclerosis. In general, SP-D shows anti-inflammatory properties, and dampens local inflammation in the vessel, as well as systemic inflammation. However, SP-D can also exert a pro-inflammatory role, as it stimulates C-C chemokine receptor 2 inflammatory blood monocytes to secrete tumor necrosis-factor α and increases secretion of interferon-γ from natural killer cells. In vivo studies examining the role of SP-D in the development of atherosclerosis agree that SP-D plays a proatherogenic role, with SP-D knockout mice having smaller atherosclerotic plaque areas, which might be caused by a decreased systemic inflammation. Clinical studies examining the association between SP-D and cardiovascular disease have reported a positive association between circulatory SP-D level, carotid intima-media thickness, and coronary artery calcification. Other studies have found that circulatory SP-D is correlated with increased risk of both total and cardiovascular disease mortality. Both in vitro, in vivo, and clinical studies examining the relationship between SP-D and CVDs will be discussed in this review.
Highlights
Cardiovascular disease (CVD) is the most frequent cause of death worldwide, with an estimated 17.9 million deaths every year, accounting for about 31% of all global deaths [1]
A positive association between circulatory surfactant protein-D (SP-D) level and carotid intima-media thickness and coronary artery calcification Circulatory surfactant protein (SP)-D is associated with a higher risk of heart transplantation, death, and worsened heart failure Circulatory SP-D is associated with more severe peripheral artery disease (PAD) and a higher prevalence of diabetes mellitus No association between plasma SP-D and carotid artery intima-media thickness or subclinical atherosclerotic plaque development Circulatory SP-D levels are increased in patients with heart failure Circulatory SP-D correlated with the presence of sub-massive pulmonary embolism
In an inflammatory environment, the dodecameric form can change to a trimeric or monomeric isoform that is believed to have pro-inflammatory properties [106] (Figure 1). This could explain the ambiguous role of SP-D as both an antiand pro-inflammatory stimulator in the development of CVD and in the absence of microbial binding
Summary
Cardiovascular disease (CVD) is the most frequent cause of death worldwide, with an estimated 17.9 million deaths every year, accounting for about 31% of all global deaths [1]. Collectins bind the cellular receptor, signal regulatory protein (SIRP)-α, on innate immune cells via their C-type lectin domain and prevent pro-inflammatory signaling. The C-type lectin domain is occupied by its corresponding ligand, and the collectins will interact with the innate immune cells through a receptor complex of cluster of differentiation (CD) and calreticulin This binding is mediated through the collagen-like domain on the collectin and induces pro-inflammatory signaling [25]. These studies underline the important roles of SP-D/-A in the pulmonary innate host defense and regulation of surfactant homeostasis [31]. A positive association between circulatory SP-D level and carotid intima-media thickness and coronary artery calcification Circulatory SP-D is associated with a higher risk of heart transplantation, death, and worsened heart failure Circulatory SP-D is associated with more severe PAD and a higher prevalence of diabetes mellitus No association between plasma SP-D and carotid artery intima-media thickness or subclinical atherosclerotic plaque development Circulatory SP-D levels are increased in patients with heart failure Circulatory SP-D correlated with the presence of sub-massive pulmonary embolism
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