Atherosclerosis: A Classic Inflammatory Disease

Anogeianaki, A.; Angelucci, Domenico; Cianchetti, Ettore; D’Alessandro, Margherita; Maccauro, Giulio; Saggini, Andrea; Salini, Vincenzo; Caraffa, Auro; Tetè, Stefano; Conti, Francesca; Tripodi, Domenico; Shaik-Dasthagirisaheb, Y.B.

doi:10.1177/039463201102400401

Cited by 55 publications

(43 citation statements)

References 61 publications

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“…It is a multifactorial disease characterized by the accumulation of cells from both the innate and acquired immune system within the intima of the arterial wall (13). Triglyceride-rich lipoproteins and free fatty acids are important factors involved in fatty streak formation and advanced atherosclerosis (14).…”

Section: Apoementioning

confidence: 99%

“…In atherosclerosis, normal homeostatic functions of the endothelium are altered, promoting an inflammatory response that results in an increased expression of adhesion molecules. This increased expression leads to the recruitment of leukocytes, including monocytes, that penetrate the intima, predisposing the vessel wall to lipid deposits (13). Reportedly, mast cells also contribute to coronary plaque progression and diet-induced obesity and diabetes through the secretion of vasoactive mediators, cytokines, and proteinases (16).…”

Section: Apoementioning

confidence: 99%

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Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Significance Apolipoprotein E −/− (ApoE −/− ) mice deficient in nucleotide binding oligomerization domain-containing protein 2 (NOD2) and subjected to an oral gavage of Porphyromonas gingivalis developed elevated serum inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis. Stimulation of NOD2 by Muramyl DiPeptide (MDP) in ApoE −/− mice reduced P. gingivalis -induced inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis by reducing the expression of inhibitor of NF-κB kinase-β, NF-κB, JNK mRNA, and TNF-α protein levels. A reduction in body weight gain was observed in ApoE −/− mice fed a high-fat diet (HFD) and injected with MDP compared to ApoE −/− mice fed a HFD but saline injected. MDP activation of NOD2 should be considered in the treatment of inflammatory processes affecting atherosclerosis, bone loss, and possibly, weight gain.

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Section: Apoementioning

confidence: 99%

Section: Apoementioning

confidence: 99%

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…In patients with acute cerebral infarction over time after onset of irreversible neurological deficits progressive worsening of symptoms, its essence is caused by atherosclerosis of carotid artery stenosis and plaque loss caused by cerebral ischemia and hypoxia pathophysiology Process [4] . Urbonaviciene et al [5] 5-year follow-up of patients with atherosclerosis associated with elevated Cys-C found that the experimental group cardiovascular mortality was significantly higher than the control group, and CRP levels are closely related and confirmed with atheroma Like sclerosis-related acute and chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Correlation Between Serum C-Reactive Protein And Cystatin C In Patients With Acute Cerebral Infarction And Carotid Artery Stenosis

et al. 2018

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To investigate the correlation between serum C-reactive protein (CRP) and serum cystatin C (Cys-C) levels in patients with acute cerebral infarction and carotid artery stenosis. Methods: From January 2015 to December 2016 admitted to our hospital new acute cerebral infarction parallel neck vascular color Doppler ultrasound examination showed 121 cases of carotid stenosis as the case group; select the same period of hospitalized patients with non-cerebrovascular disease in 50 cases As a control group. Fasting venous blood was collected on the third day after onset of the disease and serum levels of CRP and Cys-C were measured and compared. Results: Serum levels of CRP and Cys-C in case group were significantly higher than those in control group (P <0.05). The correlation between serum CRP and Cys-C was found in any pairwise comparison (r = 0.4732). The level of CRP and Cys-C were closely related to the degree of carotid artery stenosis (P <0.05). Conclusion: The combined detection of serum CRP and Cys-C levels can be used to evaluate the degree of carotid artery stenosis in patients with acute cerebral infarction and provide a reference for the next carotid endarterectomy.

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“…ACS is an inflammatory disease that involves T-cell subsets. 34 CD4 1 T cells are involved in the development of atherosclerosis and also have important effects on plaque instability. These cells can convert a chronic disease into a serious acute disorder with ensuing thromboembolism.…”

Section: The Roles Of Different Cd4mentioning

confidence: 99%

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Gao

Zhu

et al. 2013

Cell Mol Immunol

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Considerable evidence indicates that type 1 T helper (Th1)-and Th17-mediated immune responses promote the formation of atherosclerotic plaques while that CD4 1 CD25 1 Foxp3 1 regulatory T cells (Tregs) have a protective effect. However, the functions of diverse CD41 lymphocyte subsets in plaque rupture remain poorly understood because of a shortage of satisfactory plaque rupture models. Here, we established a murine model of atherosclerotic plaque rupture using a high-fat diet and collar placement on the carotid artery, and triggered plaque rupture by short-term stimulation with a combination of lipopolysaccharide, phenylephrine injection and cold in apolipoprotein E-knockout (ApoE 2/2 ) mice. We investigated the associations between Th1 cells, Th17 cells and Tregs and plaque rupture by PCR, flow cytometry, ELISA and immunohistochemistry. In total, 75% (18/24) of vulnerable plaques, but no stable plaques, showed rupture characteristics. The proportion of Th17 cells was increased among splenocytes after treatment, but the changes in the levels of Th1 cells and Tregs were not related to rupture. Furthermore, the treatment resulted in high levels of interleukin-17 (IL-17) in the serum and in the region of plaque rupture. In vitro, IL-17 increased the level of apoptosis, a major factor associated with plaque rupture, in cultured murine vascular smooth muscle cells. Th17 cells and IL-17 may be involved in the disruption of vulnerable plaques triggered by short-term stimulation with lipopolysaccharide, phenylephrine injection and cold in ApoE 2/2 mice.

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Atherosclerosis: A Classic Inflammatory Disease

Cited by 55 publications

References 61 publications

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Correlation Between Serum C-Reactive Protein And Cystatin C In Patients With Acute Cerebral Infarction And Carotid Artery Stenosis

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

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