Objective: The aim of the present study was an analysis of heteroplasmy level in mitochondrial mutations 652delG, A1555G, C3256T, T3336C, 652insG, C5178A, G12315A, G13513A, G14459A, G14846A, and G15059A in normal and affected by atherosclerosis segments of morphologically mapped aortic walls.
Methods: We investigated the 265 normal and atherosclerotic tissue sections of 5 human aortas. Intima of every aorta was divided according to morphological characteristics into segments with different types of atherosclerotic lesions: fibrous plaque, lipofibrous plaque, primary atherosclerotic lesion (fatty streak and fatty infiltration), and normal intima from human aorta. PCR-fragments were analyzed by a new original method developed in our laboratory on the basis of pyrosequence technology.
Results: According to the obtained data, mutations G12315A and G14459A are significantly associated with total and primary atherosclerotic lesions of intimal segments and lipofibrous plaques (P ≤ 0.01 and P ≤ 0.05, accordingly). Mutation C5178A is significantly associated with fibrous plaques and total atherosclerotic lesions (P ≤ 0.01). A1555G mutation shows an antiatherosclerotic effect in primary lesion in lipofibrous plaques (P ≤ 0.05). Meanwhile, G14846A mutation is antiatherogenic for lipofibrous plaques (P ≤ 0.05).
Conclusion: Therefore, mutations C5178A, G14459A, G12315A, A1555G, and G14846A were found to be associated with atherosclerotic lesions.
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http://dx.doi.org/10.1155/2015/825468 | DOI Listing |
J Inflamm Res
December 2024
Department of Cardiology, College of Medicine, Southwest Jiaotong University, Chengdu Cardiovascular Disease Research Institute, The Third People's Hospital of Chengdu, Chengdu, Sichuan, People's Republic of China.
Background: Increased levels of remnant cholesterol (RC) and inflammation are linked to higher risks of atherosclerotic cardiovascular disease. Whether a combination of C-reactive protein (CRP) and RC improves the predictive ability for evaluating the severity of coronary artery lesions remains unknown.
Methods: A total of 1675 patients with coronary artery disease were stratified according to the Synergy Between Percutaneous Coronary Intervention (SYNTAX) score (SYNTAX score ≤22 versus SYNTAX score >22).
Objective: Excess cholesterol loading on arterial macrophages is linked to foam cell formation, atherosclerosis and cardiovascular risk in rheumatoid arthritis (RA). However, the effect of changes in cholesterol loading on coronary plaque trajectory and the impact of RA therapies on this relationship are unknown. We investigated the association between variations in cholesterol loading capacity (CLC) over time and atherosclerosis progression.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Atherosclerosis and its associated cardio-cerebrovascular complications remain the leading causes of mortality worldwide. Current lipid-lowering therapies reduce only approximately one-third of the cardiovascular risk. Furthermore, vascular restenosis and thrombotic events following surgical interventions for severe vascular stenosis significantly contribute to treatment failure.
View Article and Find Full Text PDFMol Med
December 2024
Key Laboratory of Viral Pathogenesis and Infection Prevention and Control (Jinan University), Ministry of Education, School of Medicine, Jinan University, Guangzhou, 510632, China.
Rheumatoid arthritis (RA) and cardiovascular disease (CVD) are both the chronic inflammatory disease. To investigate the influence of secondary atherosclerosis on arthritis mice, we treated the ApoE mice with K/BxN serum and high fat diet (HFD), and subsequently assessed the phenotypes as well as immune profiles of K/BxN serum and HFD induced ApoE mice. We found that HFD treatment aggravated the hyperlipidemia, atherosclerotic lesions, ankle swelling and arthropathy of mice.
View Article and Find Full Text PDFCardiovasc Drugs Ther
December 2024
Department of Cardiology, Panvascular Disease Management Center (PDMC), Wenzhou Central Hospital, The Dingli Clinical College of Wenzhou Medical University, WenZhou, ZheJiang, China.
Purpose: Inflammatory responses induced by NLRP3 inflammasome contribute to the progression of atherosclerosis. This study seeks to investigate the effect of emodin on the NLRP3 inflammasome in atherogenesis and to probe the underlying mechanism.
Methods: ApoE-knockout (ApoE) mice were treated with a high-fat diet (HFD) for 12 weeks and intragastrically with emodin for 6 weeks.
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