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Effects of Endovascular Intervention on Vascular Smooth Muscle Cell Function
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Brad Winn, Bethany Acampora, Jiro Nagatomi, Martine LaBerge
Following the fatty streak theory, fatty streaks develop early in life as a result of lipid accumulation in the vessel wall caused by a high fat diet as well as genetic predisposition [6,8,9]. Early childhood lesions commonly regress but may continue to develop rapidly during the age span of 15–34 years [5,6]. In this process, LDLs are transported by transcytosis across the endothelium and deposited in the intima where a small amount may be taken up by local smooth muscle cells (SMCs) [5]. However, the LDLs may become oxidized during the process of transcytosis, thereby forming the toxic oxLDL. It is this injurious oxLDL that is thought to damage neighboring cells, thereby triggering the inflammatory response [9]. This results in local macrophage infiltration from nearby tissues as well as monocyte recruitment from the blood. The resulting macrophage population then phagocytizes the LDL. The resulting lipid-filled macrophages and SMCs form what are known as foam cells that are characteristic of atherosclerotic lesions.
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Macrophage lipid uptake may be viewed as a protective potential healing response that backfires. Ingesting oxidized lipoproteins, as well as their imperceived total chemical content such as ingesting microbes, involves the scavenging of substances perceived to be dangerous, usually containing toxic inorganic and volatile organic chemicals. Thus, oxidative stress by pollutants occurs. After lipoprotein recognition and consequent ingestion, macrophages morph into foam cells, many of which eventually die and contribute to a large lipid core, a characteristic of lesions most vulnerable to rupture.237 Surprisingly, foam-cell formation suppresses, rather than promotes, inflammatory gene expression.245 Leukocytes may fuel an inflammatory cycle, but they also, in some incarnations, quench it.
Herbal Therapies
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
H. Shahrul, M. L. Tan, A. H. Auni, S. R. Nur, S. M. N. Nurul
Berberine is an alkaloid with pharmacological effects (Neag et al., 2018). Berberine is found in numerous herbs; however, the major natural source of berberine is derived from Berberis. Alkaloid content in its bark is more than 8% with berberine as main alkaloid (Arayne et al., 2007; Imanshahidi and Hosseinzadeh, 2008). Plants rich with berberine content are used traditionally worldwide for healing ailments. Interestingly, its cardiovascular protective role includes hypotensive effects, inotropic, anti-inflammatory effects, dilation of coronary artery, anticoagulation, lowering pulse, and lowering of elevated low-density lipoprotein cholesterol (Neag et al., 2018). As a cardioprotective compound, berberine up-regulates endothelial nitric oxide synthase (eNOS) mRNA expression. It also increases production of nitric oxide (NO) from arginine. This is facilitated by the activity of eNOS. It is reported to play an important role in vasodilation (Wang et al., 2009). NO mediates the endothelium-dependent relaxation in large conduit arteries. Abnormal production of NO would cause vascular and endothelial dysfunction (Furchgott, 1999; Tawfik et al., 2006). Apart from that, the accumulation of lipid-laden foam cells initiates the progression of atherosclerosis because of augmented inflammation and impaired cholesterol metabolism within vascular walls. Berberine’s anti-atherogenic effects are manifested by suppression of ox-LDL-induced foam cell growth and cholesterol accumulation in macrophages by regulation of surtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) (Chi et al., 2014). Accumulation of fatty acid is reduced by SIRT1. It would repress PPAR-γ which is involved in atherogenesis (Picard et al., 2004). Overexpression of SIRT1 could hinder atherosclerosis by improving vascular function (Zhang et al., 2008b).
A study on the transport and interaction between blood flow and low-density-lipoprotein in near-wall regions of blood vessels
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Satyajit Choudhury, Kameswararao Anupindi, B. S. V. Patnaik
Today cardiovascular diseases are the leading cause of death globally (WHO 2017) and atherosclerosis is the root of most of these diseases. Atherosclerosis initiates with the accumulation of atherogenic lipoproteins and their aggregates in the intima of an arterial wall (Lusis 2000; Chandran et al. 2012). Its initiation is characterised by the development of cholesterol engorged macrophages known as foam cells at some preferential sites in the arteries that are dictated by blood flow dynamics. Though the foam cells or fatty streaks are not very relevant clinically, these, after a series of complex bio-chemical reactions can lead to the formation of advanced stage lesions resulting in stenosed arteries, or even worse, in the formation of thrombus due to rupture of the necrotic core of the lesion (Lusis 2000). Another pathological condition is an abdominal aortic aneurysm (AAA) which is a condition where the aortic segment just upstream of the iliac bifurcation expands irreversibly. Although, the role played by atherosclerotic plaques in the initiation and progression of the disease is not well understood, there are studies that suggest a strong correlation between high levels of low density lipoprotein (LDL) cholesterol and AAA (Harrison et al. 2018; Weng et al. 2018). Often patients with AAA were found to have atherosclerotic plaques. However, it is not clear whether this association between AAA and atherosclerosis is causal or simply due to other common risk factors (Golledge and Norman 2010).
Endocrine disrupting toxicity of aryl organophosphate esters and mode of action
Published in Critical Reviews in Environmental Science and Technology, 2023
Wenxin Hu, Peng Gao, Lei Wang, Jianying Hu
Atherosclerotic lesion formation is regulated by liver X receptors (LXRs) (Fu et al., 2001; Janowski et al., 1996; Joseph et al., 2002; Lehmann et al., 1997). Various cell types are involved in the development of AS lesions, including foam cells (i.e., cholesterol-laden macrophages), T lymphocytes, and smooth muscle cells. The genes encoding the ATP-binding cassette transporters ABCA1 and ABCG1 have been identified as LXR targets (Repa et al., 2000). These proteins function as cholesterol transporters in foam cells by mediating the intercellular transfer of cholesterol. Then high-density lipoprotein (HDL) transports cholesterol to the extracellular fluid, from which it is further transported to the liver for metabolism (Repa et al., 2002; Wilund et al., 2004).
Basic pathogenic mechanisms of atherosclerosis
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hamad Abdulsalam Hamad Alfarisi, Zenab B. Hamad Mohamed, Muhammad Bin Ibrahim
The macrophage receptor recognition shift toward LDL due to its oxidative modification causes uptake of LDL by monocyte-derived macrophages via SR that are not regulated by cholesterol content of the cell and these receptors can bind a variety of ligands such as Ox-LDL and native lipoproteins [29,32]. It is due to the function of SR there will be massive accumulation of lipids within the cytoplasm of macrophages giving picture of foamy appearance to these cells; hence, these cells have been named as foam cells and regarded as the hallmark of fatty streak [25,31,33].