Faculty Opinions recommendation of Mutations in smooth muscle alpha-actin (ACTA2) cause coronary artery disease, stroke, and Moyamoya disease, along with thoracic aortic disease.

2009 ◽  
Author(s):  
Giulio Gabbiani
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Moyamoya Disease ◽  
Aortic Disease ◽  
Thoracic Aortic Disease ◽  
Smooth Muscle Alpha Actin ◽  
Artery Disease ◽  
Alpha Actin

Abstract T P95: Coronary Artery Disease in Moyamoya Disease

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Kyung Il Jo ◽  
Jong Soo Kim ◽  
Seung-Chyul Hong ◽  
Je Young Yeon
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Moyamoya Disease ◽  
Stroke Risk ◽  
Bypass Graft ◽  
Coronary Artery Lesion ◽  
Conventional Coronary Angiography ◽  
Stroke Risk Factor ◽  
Artery Disease

Background and Purpose: Coronary artery disease in moyamoya disease (MMD) have been described sporadically in several case reports. The purpose of this study is to determine the prevalence and characteristics of coronary artery disease in patients with MMD. Methods: From August 1991 to December 2012, 446 patients diagnosed with adult MMD at our hospital. Baseline characteristics and prevalence of coronary artery disease were reviewed based on medical records and laboratory findings. The findings of conventional coronary angiography and/or coronary computed tomography were also reviewed for the presence and appearance of coronary artery lesion. Results: - Of 446 patients with adult MMD, 21 patients were found to have coronary artery disease. Ten patients were treated with coronary artery bypass graft (n=4) or percutaneous coronary intervention (n=6) for unstable angina or myocardial infarction. Eleven were treated with medication for stable angina (n=6) and variant angina with mild degree of stenosis (n=5). Median age at diagnosed with coronary artery disease of these patients were 44 (range, 27-59). Two patients showed calcification on coronary artery lesion. Comorbid stroke risk factor rate were 19%, 38%, 9.5% and 19 % in diabetes, hypertension, dyslipidemia and smoking. Six of 21 patients had more than 2 risk factor. Conclusion: - Twenty one (4.7%) of our adult MMD registry patients showed coronary artery disease. And only 2 (9.5%) showed calcification which might means that atherosclerosis burden is low in coronary artery disease with MMD. Coronary artery disease might be a clinically relevant systemic manifestation in patients with MMD, considering early onset coronary diseaes and low prevalence of stroke risk factor.

scholarly journals TGFβ, smooth muscle cells and coronary artery disease: a review

2019 ◽  
Vol 53 ◽  
pp. 90-101 ◽  
Author(s):  
Emma L. Low ◽  
Andrew H. Baker ◽  
Angela C. Bradshaw
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Artery Disease

scholarly journals Moyamoya Disease and Coronary Artery Disease. Case Report.

2001 ◽  
Vol 41 (1) ◽  
pp. 37-41 ◽  
Author(s):  
Masaki KOMIYAMA ◽  
Misao NISHIKAWA ◽  
Toshihiro YASUI ◽  
Masato OTSUKA ◽  
Kazuo HAZE
Keyword(s):  
Coronary Artery Disease ◽  
Case Report ◽  
Coronary Artery ◽  
Moyamoya Disease ◽  
Disease Case ◽  
Artery Disease

scholarly journals Associations between Vaspin Levels and Coronary Artery Disease

2020 ◽  
Vol 4 (3) ◽  
pp. 211-216
Author(s):  
Lutfu Askin ◽  
Okan Tanriverdi ◽  
Hakan Tibilli ◽  
Serdar Turkmen
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Foam Cell ◽  
Foam Cell Formation ◽  
Artery Disease

The relationship between serum vaspin levels and metabolic or coronary artery disease is currently of interest for researchers. Although adipokine concentrations have been shown to be increased significantly in atherosclerotic lesions, the role adipokines in the atherosclerotic process remains to be elucidated. Vaspin is a new biological marker associated with obesity and impaired insulin sensitivity. Plasma vaspin concentration has been shown to correlate with the severity of coronary artery disease. Vascular inflammation triggered by vaspin inhibits atherogenesis by suppressing macrophage foam cell formation and vascular smooth muscle cell migration and proliferation. Vaspin also contributes to plaque stabilization by increasing collagen content and reducing the intraplaque macrophage to vascular smooth muscle cell ratio. The therapeutic goal concerning vaspin is to fight atherosclerosis and related diseases, as well as to maintain vascular health.

scholarly journals The Emerging Role of Long Non-coding RNAs and Circular RNAs in Coronary Artery Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Mahdi Gholipour ◽  
Mohammad Taheri
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Circular Rnas ◽  
Numerous Cell ◽  
Non Coding Rnas ◽  
Artery Disease

Coronary artery disease (CAD) is a common disorder caused by atherosclerotic processes in the coronary arteries. This condition results from abnormal interactions between numerous cell types in the artery walls. The main participating factors in this process are accumulation of lipid deposits, endothelial cell dysfunction, macrophage induction, and changes in smooth muscle cells. Several lines of evidence underscore participation of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in the pathogenesis of CAD. Several lncRNAs such as H19, ANRIL, MIAT, lnc-DC, IFNG-AS1, and LEF1-AS1 have been shown to be up-regulated in the biological materials obtained from CAD patients. On the other hand, Gas5, Chast, HULC, DICER1-AS1, and MEG3 have been down-regulated in CAD patients. Meanwhile, a number of circRNAs have been demonstrated to influence function of endothelial cells or vascular smooth muscle cells, thus contributing to the pathogenesis of CAD. In the current review, we summarize the function of lncRNAs and circRNAs in the development and progression of CAD.

scholarly journals Single-Cell Genomics Reveals a Novel Cell State During Smooth Muscle Cell Phenotypic Switching and Potential Therapeutic Targets for Atherosclerosis in Mouse and Human

Circulation ◽  
2020 ◽  
Vol 142 (21) ◽  
pp. 2060-2075 ◽  
Author(s):  
Huize Pan ◽  
Chenyi Xue ◽  
Benjamin J. Auerbach ◽  
Jiaxin Fan ◽  
Alexander C. Bashore ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Single Cell ◽  
Phenotypic Switching ◽  
Atherosclerotic Plaques ◽  
Fate Mapping ◽  
Human Genomics ◽  
Single Cell Genomics ◽  
Artery Disease

Background: Smooth muscle cells (SMCs) play significant roles in atherosclerosis via phenotypic switching, a pathological process in which SMC dedifferentiation, migration, and transdifferentiation into other cell types. Yet how SMCs contribute to the pathophysiology of atherosclerosis remains elusive. Methods: To reveal the trajectories of SMC transdifferentiation during atherosclerosis and to identify molecular targets for disease therapy, we combined SMC fate mapping and single-cell RNA sequencing of both mouse and human atherosclerotic plaques. We also performed cell biology experiments on isolated SMC-derived cells, conducted integrative human genomics, and used pharmacological studies targeting SMC-derived cells both in vivo and in vitro. Results: We found that SMCs transitioned to an intermediate cell state during atherosclerosis, which was also found in human atherosclerotic plaques of carotid and coronary arteries. SMC-derived intermediate cells, termed “SEM” cells (stem cell, endothelial cell, monocyte), were multipotent and could differentiate into macrophage-like and fibrochondrocyte-like cells, as well as return toward the SMC phenotype. Retinoic acid (RA) signaling was identified as a regulator of SMC to SEM cell transition, and RA signaling was dysregulated in symptomatic human atherosclerosis. Human genomics revealed enrichment of genome-wide association study signals for coronary artery disease in RA signaling target gene loci and correlation between coronary artery disease risk alleles and repressed expression of these genes. Activation of RA signaling by all-trans RA, an anticancer drug for acute promyelocytic leukemia, blocked SMC transition to SEM cells, reduced atherosclerotic burden, and promoted fibrous cap stability. Conclusions: Integration of cell-specific fate mapping, single-cell genomics, and human genetics adds novel insights into the complexity of SMC biology and reveals regulatory pathways for therapeutic targeting of SMC transitions in atherosclerotic cardiovascular disease.

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