-
Bosnian Journal of Basic Medical... Feb 2020Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories... (Review)
Review
Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.
Topics: Adventitia; Coronary Artery Disease; Humans; Plaque, Atherosclerotic; Tunica Intima; Tunica Media
PubMed: 31465719
DOI: 10.17305/bjbms.2019.4320 -
European Heart Journal Jun 2014Vascular calcifications (VCs) are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of... (Review)
Review
Vascular calcifications (VCs) are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of the media (VCm) or intima (VCi) of the arterial wall. Both patterns of VC often coincide and occur in patients with type II diabetes, chronic kidney disease, and other less frequent disorders; VCs are also typical in senile degeneration. In this article, we review the current state of knowledge about the pathology, molecular biology, and nosology of VCm, expand on potential mechanisms responsible for poor prognosis, and expose some of the directions for future research in this area.
Topics: Adult; Arteriosclerosis; Biomarkers; Calcium-Binding Proteins; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Female; Humans; Hyperphosphatemia; Male; Monckeberg Medial Calcific Sclerosis; Phosphates; Prognosis; Renal Insufficiency, Chronic; Terminology as Topic; Tunica Intima; Tunica Media; Vascular Calcification
PubMed: 24740885
DOI: 10.1093/eurheartj/ehu163 -
Journal of the American College of... May 2020Medium-sized and large arteries consist of 3 layers: the tunica intima, tunica media, and tunica adventitia. The tunica media accounts for the bulk of the vessel wall... (Review)
Review
Medium-sized and large arteries consist of 3 layers: the tunica intima, tunica media, and tunica adventitia. The tunica media accounts for the bulk of the vessel wall and is the chief determinant of mechanical compliance. It is primarily composed of circumferentially arranged layers of vascular smooth muscle cells that are separated by concentrically arranged elastic lamellae; a form of extracellular matrix (ECM). The tunica media is separated from the tunica intima and tunica adventitia, the innermost and outermost layers, respectively, by the internal and external elastic laminae. This second part of a 4-part JACC Focus Seminar discusses the contributions of the ECM to vascular homeostasis and pathology. Advances in genetics and proteomics approaches have fostered significant progress in our understanding of vascular ECM. This review highlights the important role of the ECM in vascular disease and the prospect of translating these discoveries into clinical disease biomarkers and potential future therapies.
Topics: Animals; Cardiology; Endothelium, Vascular; Extracellular Matrix; Humans; Muscle, Smooth, Vascular; Vascular Diseases
PubMed: 32354385
DOI: 10.1016/j.jacc.2020.03.018 -
Bosnian Journal of Basic Medical... Aug 2018In coronary artery disease (CAD), the disruption of the tunica media immune privilege manifests as increased leukocyte infiltration and the formation of vasa vasorum. We...
In coronary artery disease (CAD), the disruption of the tunica media immune privilege manifests as increased leukocyte infiltration and the formation of vasa vasorum. We aimed to characterize the immune privilege status of the tunica media in human coronary arteries (CAs) with atherosclerotic plaques, by comparing the abundance and composition of immune-cell infiltrates within the individual arterial-wall layers, and by evaluating vasa vasorum neovascularization of the tunica media. The tissue samples were obtained from 36 symptomatic patients with diffuse CAD (aged 60-72 years) who underwent coronary endarterectomy. T and B cells, macrophages and endothelial cells in the CAs were detected by immunohistochemistry. Morphological analysis of CAs showed significant atherosclerotic changes in all specimens. In the media, we observed damage and loss of smooth muscle cells, destruction of the extracellular matrix architecture, and fibrosis. There were 43.3% of immune cells in the intima, 50% in the adventitia, and 6.7% in the media. In the media, 51.1% of the immune cells were T cells (p ˂ 0.001 compared to B cells and macrophages; ANOVA, Scheffe post hoc analysis), 23.5% were B cells, and 25.4% were macrophages. The number of vasa vasorum in the media was 1 in 38.9% of CAs, 2-3 in 36.1%, and ≥4 in 25% of CAs. Our results indicate that, in atherosclerotic CAs, the immune privilege of the media is disrupted by the infiltration of T and B cells, macrophages, and the presence of vasa vasorum.
Topics: Aged; Atherosclerosis; B-Lymphocytes; Cell Proliferation; Coronary Vessels; Endothelial Cells; Humans; Immunohistochemistry; Leukocytes; Macrophages; Middle Aged; Plaque, Atherosclerotic; T-Lymphocytes; Tunica Media; Vasa Vasorum
PubMed: 29671719
DOI: 10.17305/bjbms.2018.2951 -
Chinese Medical Journal May 2017Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of... (Review)
Review
OBJECTIVE
Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosclerotic calcification) or tunica media (Mönckenberg's sclerosis). Vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.
DATA SOURCES
We conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords "genetics and vascular calcification", "molecular pathways, genetic and vascular calcification" and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.
STUDY SELECTION
The most valuable published original and review articles related to our objective were selected.
RESULTS
Vascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development.
CONCLUSION
Although several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease.
Topics: Diabetes Mellitus; Dyslipidemias; Humans; Kidney Failure, Chronic; Renal Insufficiency, Chronic; Tunica Intima; Tunica Media; Vascular Calcification
PubMed: 28469108
DOI: 10.4103/0366-6999.204931 -
Basic & Clinical Pharmacology &... Jan 2012Arterioles are the blood vessels in the arterial side of the vascular tree that are located proximal to the capillaries and, in conjunction with the terminal arteries,... (Review)
Review
Arterioles are the blood vessels in the arterial side of the vascular tree that are located proximal to the capillaries and, in conjunction with the terminal arteries, provide the majority of resistance to blood flow. Consequently, arterioles are important contributors to the regulation of mean arterial pressure and tissue perfusion. Their wall consists of cellular and extracellular components that have been traditionally classified as conforming three layers: an intima containing endothelial cells sited on a basement membrane; a media made of an internal elastic lamina apposed by one or two layers of smooth muscle; and an adventitia composed mostly of collagen bundles, nerve endings and some fibroblasts. These components of the arteriolar wall are dynamically interconnected, providing a level of plasticity to the arteriolar wall that blurs the traditional boundaries of a rigid layered classification. This MiniReview focuses on the structural conformation of the arteriolar wall and shows how wall components interact spatially, functionally and temporally to control vascular diameter, regulate blood flow and maintain vascular permeability.
Topics: Animals; Arterioles; Capillary Permeability; Connective Tissue; Connective Tissue Cells; Humans; Tunica Intima; Tunica Media; Vascular Resistance
PubMed: 21989114
DOI: 10.1111/j.1742-7843.2011.00813.x -
PloS One 2020Aging causes stiffness and decreased function of the renal artery (RA). Histological study with light microscopy can reveal microscopic structural remodeling but no...
OBJECTIVES
Aging causes stiffness and decreased function of the renal artery (RA). Histological study with light microscopy can reveal microscopic structural remodeling but no functional changes. The present study aimed to clarify the association between structural and functional aging of the RA through the use of scanning acoustic microscopy.
METHODS
Formalin-fixed, paraffin-embedded cross-sections of renal arteries from 64 autopsy cases were examined. Speed-of-sound (SOS) values of three layers, which correspond to the stiffness, were compared among different age groups. SOS of the tunica media was examined in terms of blood pressure (BP) and SOS of the ascending aorta. Vulnerability to proteases was assessed by SOS reduction after collagenase treatment.
RESULTS
The tunica intima presented inward hypertrophy with luminal narrowing, and the tunica media showed outward hypertrophic remodeling with aging. SOS of the tunica media and internal and external elastic laminae showed a reverse correlation with age. SOS of the tunica media was negatively correlated with BP and strongly associated with that of the aorta. The tunica media of young RAs were more sensitive to collagenase compared with the old ones.
CONCLUSIONS
Scanning acoustic microscopy is useful for observing the aging process of the RA. This technique simultaneously shows structural and mechanical information from each portion of the RA. In the process of aging, the RA loses contractile function and elasticity as a result of protease digestion. The tunica media and the internal and external elastic laminae exhibit reduced stiffness, but the tunica intima stiffens with atherosclerosis. As a consequence, the RA's outer shape changes from round to oval with inward and outward hypertrophy. This indicates that the inner resistant intima supports the mechanical weakness of the tunica media to compensate for an increase in BP with aging.
Topics: Adult; Aged, 80 and over; Aging; Autopsy; Blood Pressure; Female; Humans; Male; Microscopy, Acoustic; Renal Artery; Tunica Intima; Tunica Media
PubMed: 33147291
DOI: 10.1371/journal.pone.0234759 -
Arteriosclerosis, Thrombosis, and... Nov 2020There is no medical treatment to prevent abdominal aortic aneurysm (AAA) growth and rupture, both of which are linked to smoking. Our objective was to map the...
OBJECTIVE
There is no medical treatment to prevent abdominal aortic aneurysm (AAA) growth and rupture, both of which are linked to smoking. Our objective was to map the tunica-specific pathophysiology of AAA with consideration of the intraluminal thrombus, age, and sex, and to subsequently identify which mechanisms were linked to smoking and diameter growth rate. Approach and Results: Microarray analyses were performed on 246 samples from 76 AAA patients and 13 controls. In media and adventitia, there were 5889 and 2701 differentially expressed genes, respectively. Gene sets related to adaptive and innate immunity were upregulated in both tunicas. Media-specific gene sets included increased matrix disassembly and angiogenesis, as well as decreased muscle cell development, contraction, and differentiation. Genes implicated in previous genome-wide association studies were dysregulated in media. The intraluminal thrombus had a pro-proteolytic and proinflammatory effect on the underlying media. Active smoking resulted in increased inflammation, oxidative stress, and angiogenesis in all tissues and enriched lipid metabolism in adventitia. Processes enriched with active smoking in control aortas overlapped to a high extent with those differentially expressed between AAAs and controls. The AAA diameter growth rate (n=24) correlated with T- and B-cell expression in media, as well as lipid-related processes in the adventitia.
CONCLUSIONS
This tunica-specific analysis of gene expression in a large study enabled the detection of features not previously described in AAA disease. Smoking was associated with increased expression of aneurysm-related processes, of which adaptive immunity and lipid metabolism correlated with growth rate.
Topics: Adaptive Immunity; Adult; Aged; Aorta, Abdominal; Aortic Aneurysm, Abdominal; Case-Control Studies; Dilatation, Pathologic; Disease Progression; Female; Gene Regulatory Networks; Gene-Environment Interaction; Humans; Lipid Metabolism; Male; Middle Aged; Risk Factors; Smoking; Thrombosis; Transcriptome; Tunica Media; Vascular Remodeling
PubMed: 32907367
DOI: 10.1161/ATVBAHA.120.314264 -
F1000Research 2018Almost 50 years ago, Earl Benditt and his son John described the clonality of the atherosclerotic plaque. This led Benditt to propose that the atherosclerotic lesion was... (Review)
Review
Almost 50 years ago, Earl Benditt and his son John described the clonality of the atherosclerotic plaque. This led Benditt to propose that the atherosclerotic lesion was a smooth muscle neoplasm, similar to the leiomyomata seen in the uterus of most women. Although the observation of clonality has been confirmed many times, interest in the idea that atherosclerosis might be a form of neoplasia waned because of the clinical success of treatments for hyperlipemia and because animal models have made great progress in understanding how lipid accumulates in the plaque and may lead to plaque rupture. Four advances have made it important to reconsider Benditt's observations. First, we now know that clonality is a property of normal tissue development. Second, this is even true in the vessel wall, where we now know that formation of clonal patches in that wall is part of the development of smooth muscle cells that make up the tunica media of arteries. Third, we know that the intima, the "soil" for development of the human atherosclerotic lesion, develops before the fatty lesions appear. Fourth, while the cells comprising this intima have been called "smooth muscle cells", we do not have a clear definition of cell type nor do we know if the initial accumulation is clonal. As a result, Benditt's hypothesis needs to be revisited in terms of changes in how we define smooth muscle cells and the quite distinct developmental origins of the cells that comprise the muscular coats of all arterial walls. Finally, since clonality of the lesions is real, the obvious questions are do these human tumors precede the development of atherosclerosis, how do the clones develop, what cell type gives rise to the clones, and in what ways do the clones provide the soil for development and natural history of atherosclerosis?
Topics: Animals; Clone Cells; Humans; Myocytes, Smooth Muscle; Plaque, Atherosclerotic; Tunica Intima; Tunica Media
PubMed: 30613386
DOI: 10.12688/f1000research.15994.1 -
American Journal of Hypertension Sep 2018Morphological and physiological changes in the vasculature have been described in the evolution and maintenance of hypertension. Hypertension-induced vascular... (Review)
Review
Morphological and physiological changes in the vasculature have been described in the evolution and maintenance of hypertension. Hypertension-induced vascular dysfunction may present itself as a contributing, or consequential factor, to vascular remodeling caused by chronically elevated systemic arterial blood pressure. Changes in all vessel layers, from the endothelium to the perivascular adipose tissue (PVAT), have been described. This mini-review focuses on the current knowledge of the structure and function of the vessel layers, specifically muscular arteries: intima, media, adventitia, PVAT, and the cell types harbored within each vessel layer. The contributions of each cell type to vessel homeostasis and pathophysiological development of hypertension will be highlighted.
Topics: Adipose Tissue; Animals; Arterial Pressure; Arteries; Humans; Hypertension; Tunica Intima; Tunica Media; Vascular Remodeling
PubMed: 29788246
DOI: 10.1093/ajh/hpy083