scholarly journals Inflammation in Atherosclerosis: From Theory to Practice

2020 ◽  
Vol 6 (10) ◽  
pp. 186-205
Author(s):  
A. Chaulin ◽  
Ju. Grigoryeva

Inflammation causes the formation, progression, and rupture of atherosclerotic plaques, which are an integral part of cardiovascular diseases. Numerous components are involved in the pathogenesis of atherosclerotic inflammation. Experimental studies have shown that the inflammatory subpopulation of monocytes / macrophages mainly accumulates in the atherosclerotic plaque and produces Pro-inflammatory cytokines that enhance atherogenesis. T-lymphocytes can contribute to the inflammatory processes that contribute to thrombosis by stimulating the production of collagen-destroying proteinases and a powerful procoagulant substance, tissue factor. Many research data link obesity, inflammation, and risk factors for atherosclerosis, which is a growing clinical concern given the increasing prevalence of obesity worldwide. Modulators of inflammation originating from visceral adipose tissue cause the liver to produce acute phase reagents involved in thrombosis. Additionally, levels of C-reactive protein increase with increasing levels of visceral adipose tissue. The adipose tissue of obese mice contains an increased number of macrophages and T-lymphocytes, increased activation of T-lymphocytes, and increased expression of interferon-gamma. It was found that interferon-gamma deficiency in mice reduces the production of inflammatory cytokines and the accumulation of inflammatory cells in adipose tissue. Another series of experiments on mice in vitro and in vivo confirmed that adiponectin, an adipocytokine whose plasma levels drop with obesity, acts as an endogenous anti-inflammatory modulator of both innate and acquired immunity in atherogenesis. Thus, the accumulation of experimental data confirms the key role of inflammation as a link between risk factors for atherosclerosis and the biology underlying the complications of this disease. A large Jupiter clinical trial confirms the clinical utility of assessing inflammatory status in therapeutic interventions to limit cardiovascular events. Thus, knowledge of the pathogenetic mechanisms underlying atherosclerotic inflammation is not only of theoretical value, but can also be used in practice when assessing the risk and prescribing therapy.

2016 ◽  
Vol 252 ◽  
pp. e182
Author(s):  
R. Poledne ◽  
I. Kralova Lesna ◽  
A. Kralova ◽  
A. Sekerkova ◽  
J. Fronek

1998 ◽  
Vol 133 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Scott Owens ◽  
Bernard Gutin ◽  
Michael Ferguson ◽  
Jerry Allison ◽  
Warren Karp ◽  
...  

2016 ◽  
Vol 42 (2) ◽  
pp. 86-95 ◽  
Author(s):  
Anawin Sanguankeo ◽  
Mariana Lazo ◽  
Sikarin Upala ◽  
Frederick L. Brancati ◽  
Susanne Bonekamp ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Adèle Lasbleiz ◽  
Bénédicte Gaborit ◽  
Astrid Soghomonian ◽  
Axel Bartoli ◽  
Patricia Ancel ◽  
...  

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the “cytokine storm” and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.


2017 ◽  
Vol 71 (1) ◽  
pp. 0-0
Author(s):  
Agnieszka Owczarczyk-Saczonek ◽  
Waldemar Placek

Many epidemiological studies have confirmed the relationship of obesity and psoriasis, and it is believed that obesity is an independent risk factor for its development and is associated with a worse prognosis. Furthermore, the reduction of body weight, using low-calorie diet combined with exercise, reduces the severity of psoriasis.Visceral adipose tissue is the largest endocrine organ, producing proinflammatory cytokines (TNF-α, IL-6, IL-17) and adipokines (adiponectin, omentin, chemerin). They participate in the development of dyslipidemia, insulin resistance, diabetes, and consequently of the cardiovascular diseases. Macrophages of visceral adipose tissue have a special role and they increase significantly in obesity. They are responsible for the development of inflammation in adipose tissue and produce inflammatory cytokines (TNF alpha, IL-6, Il-8, Il-17, Il-18, MCP-1) and other adipokines: resistin, visfatin, retinol-binding protein 4. This explains the concept of «psoriatic march «and observations of the frequent coexistence of psoriasis with obesity. Inflammation associated with systemic disease, fanned by pro-inflammatory cytokines and adipokines produced by the visceral adipose tissue lead to the development of insulin resistance, endothelial cell damage. Endothelial dysfunction predisposes to the formation of atherosclerotic plaques and faster development of cardiovascular events. Complication of obesity is the development of non-alcoholic fatty liver disease (NAFLD), which states twice as likely in patients with plaque psoriasis and is associated with the severity of the disease. Another consequence is the development of depression. Probably the proinflammatory cytokines can interact with metabolism of neurotransmitters. Obesity also has a significant impact on the treatment of psoriasis, increasing the risk of adverse effects of systemic drugs, reducing the efficacy of biological agents which dose should be adjusted to the weight of the patient. It is a factor responsible for the increased volume of distribution and it causes low titter of drug concentration.


2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Wook Yi ◽  
Keunyoung Kim ◽  
Myungsoo Im ◽  
Soree Ryang ◽  
Eun Heui Kim ◽  
...  

AbstractWe evaluated the associations between metabolic parameters with visceral adipose tissue (VAT) volume in women with prediabetes or type 2 diabetes (T2DM), and we compared the VAT volume with the VAT area. We enrolled women aged > 20 years with prediabetes or T2DM, who underwent oral glucose tolerance test and whose VAT was evaluated using computed tomography (CT) at our institution between 2017 and 2019. All participants underwent unenhanced spiral CT with a 3-mm slice thickness from the level of the diaphragm to the level of the mid-thigh. The two VAT areas were defined as the free drawn area on the levels of the umbilicus and L2 vertebra. The VAT areas were also manually drawn from the level of the diaphragm to the level of the pelvic floor and were used to calculate the VAT volumes by summing all areas with a slice thickness of 3 mm after setting the attenuation values from −45 to −195 Hounsfield Unit. All metabolic characteristics, except blood pressure, were significantly correlated with the VAT volume. The VAT areas measured at the level of the L2 vertebra and umbilicus were correlated with serum triglyceride, high-density lipoprotein cholesterol, and Framingham steatosis index alone. Multivariable regression analyses revealed that the VAT volume was significantly associated with several metabolic parameters. In conclusion, in women with prediabetes and T2DM, the VAT volume acquired from CT-based calculation has more significant correlations with metabolic risk factors compared with the VAT area.


2019 ◽  
Vol 8 (1) ◽  
pp. R1-R9 ◽  
Author(s):  
Alessandra Gambineri ◽  
Carla Pelusi

An imbalance in sex hormones has an important impact on type 2 diabetes (T2DM) mainly through the involvement of visceral adipose tissue. Androgens have an interesting sex-dimorphic association with T2DM, since hyperandrogenism in females and hypogonadism in males are risk factors for T2DM. Thus, treatments aimed at correcting hyperandrogenism in females and hypogonadism in males may prevent the development of T2DM or help in its treatment.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Satoshi Nishimura ◽  
Mika Nagasaki ◽  
Ichiro Manabe ◽  
Kinya Seo ◽  
Takashi Kadowaki ◽  
...  

Metabolic syndrome is a major risk factor of cardiovascular events, and obese visceral adipose tissue remodeling and malfunctioning based on chronic inflammation plays a central role. To assess dynamic multi-cellular interplay, a novel ex vivo (a–c) and in vivo (d–f) adipose tissue imaging method was developed. We found close spatial and temporal interrelationships between angiogenesis and adipogenesis, and both were augmented in obese adipose (c,arrow). In addition, we found increased leukocyte-platelet-endothelial cell interactions in the micro-circulation of obese visceral adipose that were indicative of activation of the leukocyte adhesion cascade, a hallmark of inflammation (e,f). Both macrophages and endothelial cells showed increased adhesion molecules including ICAM-1 and Selectin families, and P-selectin positive platelets were increased locally in obese adipose. Up-regulated expression of adhesion molecules on multiple cell types suggests their increased interactions contribute to local activation of inflammatory processes within visceral obese adipose tissue. Interestingly, the heightened leukocyte-platelet-endothelial interactions were not observed in obese subcutaneous fat pads. Our results demonstrated the power of our imaging technique to analyze complex inflammatory cellular interplays in vivo and to evaluate new therapeutic interventions against them. Results also indicate that visceral adipose tissue obesity is an inflammatory disease.


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