scholarly journals Relationship between ADAMTS4 and carotid atherosclerotic plaque vulnerability in humans

2018 ◽  
Vol 67 (4) ◽  
pp. 1120-1126 ◽  
Author(s):  
Honglin Dong ◽  
Tian Du ◽  
Shyamal Premaratne ◽  
Cynthia X. Zhao ◽  
Qinqin Tian ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Vulnerability

Computational Plaque Vulnerability Index for Atherosclerotic Carotid Plaque Assessment Based on In Vivo MR-Image

2008 ◽  
Author(s):  
Zhongzhao Teng ◽  
Xueying Huang ◽  
Chun Yuan ◽  
Gador Canton ◽  
Fei Liu ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Plaque ◽  
Vulnerability Index ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Vulnerability ◽  
Mr Image ◽  
Noninvasive Methods ◽  
Screening And Diagnosis

Carotid atherosclerotic plaque (CAP) may rupture without warning and cause acute cardiovascular syndromes such as stroke, which is the No.3 killer in USA and a leading cause of serious disabilities. Available screening and diagnosis techniques are insufficient to identify those victims before the event occurs. Noninvasive methods to identify new and emerging biomarkers to assess plaque vulnerability and predict possible rupture before the fatal event are urgently called for.

scholarly journals Correlation Between Calcification Characteristics of Carotid Atherosclerotic Plaque and Plaque Vulnerability

2021 ◽  
Vol Volume 17 ◽  
pp. 679-690
Author(s):  
Xiangli Xu ◽  
Yang Hua ◽  
Beibei Liu ◽  
Fubo Zhou ◽  
Lili Wang ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Vulnerability

scholarly journals Histone Deacetylase 9 Activates IKK to Regulate Atherosclerotic Plaque Vulnerability

2020 ◽  
Vol 127 (6) ◽  
pp. 811-823 ◽  
Author(s):  
Yaw Asare ◽  
Thomas A. Campbell-James ◽  
Yury Bokov ◽  
Lydia Luya Yu ◽  
Matthias Prestel ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Atherosclerotic Plaque ◽  
Association Studies ◽  
Endothelial Activation ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Plaque Vulnerability ◽  
Plaque Stability ◽  
Genome Wide ◽  
Histone Deacetylase 9

Rationale: Arterial inflammation manifested as atherosclerosis is the leading cause of mortality worldwide. Genome-wide association studies have identified a prominent role of HDAC (histone deacetylase)-9 in atherosclerosis and its clinical complications including stroke and myocardial infarction. Objective: To determine the mechanisms linking HDAC9 to these vascular pathologies and explore its therapeutic potential for atheroprotection. Methods and Results: We studied the effects of Hdac9 on features of plaque vulnerability using bone marrow reconstitution experiments and pharmacological targeting with a small molecule inhibitor in hyperlipidemic mice. We further used 2-photon and intravital microscopy to study endothelial activation and leukocyte-endothelial interactions. We show that hematopoietic Hdac9 deficiency reduces lesional macrophage content while increasing fibrous cap thickness thus conferring plaque stability. We demonstrate that HDAC9 binds to IKK (inhibitory kappa B kinase)-α and β, resulting in their deacetylation and subsequent activation, which drives inflammatory responses in both macrophages and endothelial cells. Pharmacological inhibition of HDAC9 with the class IIa HDAC inhibitor TMP195 attenuates lesion formation by reducing endothelial activation and leukocyte recruitment along with limiting proinflammatory responses in macrophages. Transcriptional profiling using RNA sequencing revealed that TMP195 downregulates key inflammatory pathways consistent with inhibitory effects on IKKβ. TMP195 mitigates the progression of established lesions and inhibits the infiltration of inflammatory cells. Moreover, TMP195 diminishes features of plaque vulnerability and thereby enhances plaque stability in advanced lesions. Ex vivo treatment of monocytes from patients with established atherosclerosis reduced the production of inflammatory cytokines including IL (interleukin)-1β and IL-6. Conclusions: Our findings identify HDAC9 as a regulator of atherosclerotic plaque stability and IKK activation thus providing a mechanistic explanation for the prominence of HDAC9 as a vascular risk locus in genome-wide association studies. Its therapeutic inhibition may provide a potent lever to alleviate vascular inflammation. Graphical Abstract: A graphical abstract is available for this article.

Evaluating intensity normalization for multispectral classification of carotid atherosclerotic plaque

2015 ◽  
Author(s):  
Shan Gao ◽  
Ronald van’t Klooster ◽  
Diederik F. van Wijk ◽  
Aart J. Nederveen ◽  
Boudewijn P. F. Lelieveldt ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Atherosclerotic Plaque ◽  
Intensity Normalization

Differentiation of Vulnerable Carotid Plaques by Analysis of Calcium Content and Spectral Curve Slope using Gemstone Spectral Imaging

2021 ◽  
Author(s):  
Ze-Xin Fan ◽  
Xiao-Qing Li ◽  
Ting-Ting Yang ◽  
Shao-Jie Yuan ◽  
Tian-Tong Niu ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Plaque ◽  
Spectral Curve ◽  
Plaque Rupture ◽  
Spectral Imaging ◽  
Calcium Content ◽  
Carotid Atherosclerotic Plaque ◽  
Close Link ◽  
Gemstone Spectral Imaging ◽  
Hs Crp

Abstract Growing evidence indicates that vulnerable carotid plaque rupture is an important cause of stroke. However, fewer studies have been conducted to investigate the role of a novel gemstone spectral imaging (GSI) in assessment of vulnerable carotid plaque. In this study, we analyzed GSI data including calcium content of carotid atherosclerotic plaque and spectral curve slope, as well as serum high-sensitivity C-reactive protein (Hs-CRP), monocyte chemotactic protein-1 (MCP-1) levels in patients with carotid atherosclerotic plaque using the GSI-computed tomographic angiography (CTA) and immunoturbidimetry. The patients with unstable plaques demonstrated a significantly lower calcium content and higher spectral curve slope than the stable plaques group. In addition, the patients with unstable plaque showed an increase in Hs-CRP levels and MCP-1 levels compared with the stable plaque and normal controls (NC) group. The alternation in GSI calcium content and spectral curve slope reflects a close link between calcification and plaque instability, while derangement of Hs-CRP and MCP-1 is involved in the formation or development of vulnerable plaques. Taken together, our results strongly support the feasibility of using these serological and newly discovered imaging parameters as multiple potential biomarkers relevant to plaque vulnerability or stroke progression.

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