Atherosclerosis is a leading cause of death worldwide, and its mechanisms are still unclear. However, various animal models have significantly advanced our understanding of the mechanisms involved in atherosclerosis and have allowed the evaluation of therapeutic options. The aim of this paper is to review those animal models (i.e., rabbits, mice, rats, guinea pigs, hamsters, avian, carnivores, swine, and, non-human primates) that have been used to study atherosclerosis. Though there is no single perfect animal model that completely replicates the stages of human atherosclerosis, cholesterol feeding and mechanical endothelial injury are two common features shared by most models of atherosclerosis. Further, with the development of genetically modified animals, these models are significantly broadening our understanding of the pathogenesis of atherosclerosis.
Animals ; Atherosclerosis ; epidemiology ; metabolism ; pathology ; Disease Models, Animal ; Humans

CD36 is a membrane glycoprotein that is present on various types of cells, including monocytes, macrophages, microvascular endothelial cells, adipocytes and platelets. Macrophage CD36 participates in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL), which triggers signaling cascades for inflammatory responses. CD36 functions in oxLDL uptake and foam cell formation, which is the initial critical stage of atherosclerosis. In addition, oxLDL via CD36 inhibits macrophage migration, which may be a macrophage-trapping mechanism in atherosclerotic lesions. The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation. Platelet CD36 also promotes atherosclerotic inflammatory processes and is involved in thrombus formation after atherosclerotic plaque rupture. Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.
Animals ; Antigens, CD36/chemistry/genetics/*metabolism ; Atherosclerosis/*metabolism/pathology ; Humans ; Macrophages/metabolism/pathology ; Plaque, Atherosclerotic/*metabolism/pathology

The effect of adventitia on the occurrence and development of atherosclerosis (As) is getting more attentions. Fibroblasts, mast cells, dendritic cells, vasa vasorums, vascular-associated lymphoid tissues, and vascular peripheral nerves are related to the occurrence and development of As. This essay summarizes studies on the changes in adventitia in As process and its effect on the occurrence and development of As, as well as the latest progress.
Adventitia ; drug effects ; metabolism ; pathology ; Animals ; Atherosclerosis ; drug therapy ; metabolism ; pathology ; Disease Progression ; Humans

AIMTo study the expressions of scavenger receptor class B type I(SR-BI) and peroxisome proliferator-activated receptor gamma (PPARgamma) in atherosclerotic mini swine and provide a new mechanism for investigating the pathogenesis of atherosclerosis.

METHODSChinese mini swine were fed by a normal control diet or a high fat/high cholesterol diet for 12 months after common carotid artery injury induced by balloon denudation. Plasma total cholesterol(TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were determined by commercially enzymatic methods every two months. The sections, which were taken from liver and abdominal aorta, were stained with hematoxylin eosin. The expressions of SR-BI and PPARgamma mRNA and protein in liver and aorta tissue were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry respectively.

RESULTSAt the end of 12 months, plasma TC, HDL-C and TG in HFHC mini swine were increased. There were fatty liver and atherosclerotic plaque in mini swine live and aorta respectively. The expression of SR-BI was upregulated in HFHC mini swine liver and aorta tissue.

CONCLUSIONHFHC may induce atherosclerosis and the expression of SR-BI and PPARgamma. Upregulating SR-BI expression may inhibit atherosclerosis. Increasing SR-BI expression in liver and aorta may accelerate SR-BI-mediated reverse cholesterol transport and develop a new anti-atherogenic strategy.

Animals ; Arteriosclerosis ; pathology ; Atherosclerosis ; metabolism ; PPAR gamma ; metabolism ; Receptors, Scavenger ; metabolism ; Swine

Atherosclerosis ; pathology ; C-Reactive Protein ; metabolism ; Dendritic Cells ; metabolism ; Glycation End Products, Advanced ; metabolism ; Humans ; Inflammation

Gap junctions play a critical role in electrical synchronization and exchange of small molecules between neighboring cells; connexins are a family of structurally related transmembrane proteins that assemble to form vertebrate gap junctions. Hyperglycemia changes the structure gap junction proteins and their expression, resulting in obstruction of neural regeneration, vascular function and wound healing, and also promoting vascular atherosclerosis. These pathogenic factors would cause diabetic foot ulcers. This article reviews the involvement of connexins in pathogenesis of diabetic foot.
Atherosclerosis ; Connexins ; metabolism ; Diabetic Foot ; pathology ; Gap Junctions ; metabolism ; Humans ; Hyperglycemia ; physiopathology ; Regeneration ; Wound Healing

OBJECTIVETo observe the urokinase receptor (uPAR) expression in atherosclerotic plaques of human femoral arteries.

METHODSHuman femoral artery samples were collected from patients underwent femoral endarterectomy. Normal internal mammary artery samples were taken from bypass surgery served as control. uPAR protein distribution at shoulders, lipid pool and rupture sites of a plaque and the association with macrophages and smooth muscle cells (SMCs) were detected by immunohistochemistry methods.

RESULTSThere was no uPAR expression in intima or tunica media of normal internal mammary arteries. In atherosclerotic lesions of femoral artery, the mean optical density (A) of uPAR was 92 +/- 37 in intima and 46 +/- 28 in tunica media (P < 0.05). The intimal uPAR was coexisted with macrophages and SMCs. uPAR expression was observed at plaque shoulders and lipid pool, while the maximal expression was found at rupture sites.

CONCLUSIONThe increased expression of uPAR in atherosclerotic lesion and uPAR distribution at shoulders, lipid pool, as well as rupture sites of plaques suggest a role of uPAR in plaque rupture process.

Atherosclerosis ; metabolism ; pathology ; Endarterectomy ; Femoral Artery ; pathology ; Humans ; Receptors, Urokinase Plasminogen Activator ; metabolism ; Urokinase-Type Plasminogen Activator ; metabolism

Accumulating evidences have documented that angiogenesis is closely linked to inflammation and regulators of angiogenesis play key roles in various inflammatory conditions. PlGF is an angiogenic protein belonging to the VEGF family and is upregulated mainly in pathologic conditions. Recently, PlGF was discovered having a proinflammatory role in inflammatory arthritis and its serum level drew attention not only as a useful surrogate biomarker but also a potential therapeutic target in atherosclerosis and various cancers. Particularly, PlGF has attractive clinical values because endogenous PlGF is redundant for vascular development and physiological vessel maintenance in healthy adults. However, there have been conflicting results about the efficacy of PlGF inhibition depending on the experimental and clinical settings. Further close investigations for resolving the puzzle of PlGF biology are required.
Animals ; Arthritis, Rheumatoid/*metabolism/pathology ; Atherosclerosis/*metabolism/pathology ; Biological Markers/metabolism ; Humans ; Inflammation/metabolism ; Neoplasms/*metabolism/pathology ; Neovascularization, Pathologic ; Pregnancy Proteins/*metabolism ; Signal Transduction

Atherosclerosis is an important pathological basis for coronary artery disease. ANRIL is an antisense non-coding RNA located in Chr9p21 locus, which was identified as the most significant risk locus associated with atherosclerosis. ANRIL can produce multiple transcripts including linear and circular transcripts after various transcript splicing. It has been illustrated that ANRIL plays important roles in the pathology of atherosclerosis by regulating the proliferation and apoptosis of vascular cells. Linear ANRIL can regulate the proliferation of vascular smooth muscle cells (VSMCs) in plaques by chromatin modification, as well as influence the proliferation and the apoptosis of macrophages in post transcription; circular ANRIL can affect the proliferation and apoptosis of VSMCs by chromatin modification as well as interfering with rRNA maturation. In this review, we describe the ANRIL evolution, different transcripts characteristics, and their roles in the proliferation and apoptosis of vascular cells to participate in the process of atherosclerosis, for further understanding the pathogenesis of atherosclerosis and finding potential targets for diagnosis and treatment of atherosclerosis.
Apoptosis ; genetics ; Atherosclerosis ; genetics ; Cell Proliferation ; genetics ; Humans ; Myocytes, Smooth Muscle ; pathology ; RNA, Long Noncoding ; metabolism

Atherosclerosis ; immunology ; metabolism ; pathology ; Biomarkers ; metabolism ; C-Reactive Protein ; metabolism ; Endothelium, Vascular ; metabolism ; pathology ; physiopathology ; Inflammation ; metabolism ; pathology ; Inflammation Mediators ; metabolism ; Interleukins ; metabolism ; Metabolic Syndrome ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism