This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
Mitochondrial dysfunction fuels vascular inflammation and atherosclerosis. However, the role of MICU1 in vascular inflammation and atherosclerosis remains unknown. Here, we report that endothelial MICU1 prevents vascular inflammation and atherosclerosis by maintaining mitochondrial homeostasis.
Atherosclerosis, or the buildup of plaque in the arteries, develops when low-density lipoprotein cholesterol (LDL-C) enters the blood vessel walls through dysfunctional endothelial cells (EC), leading to the formation of plaques.
Researchers show that genetic traits influence the cellular composition of atherosclerotic plaques, which over time will affect the risk of such lesions to cause a stroke or heart attack. The new knowledge can be used to improve the risk assessment and treatment of patients with atherosclerosis in the future.
University of Virginia School of Medicine researchers have created an "atlas of atherosclerosis" that reveals, at the level of individual cells, critical processes responsible for forming the harmful plaque buildup that causes heart attacks, strokes, and coronary artery disease.
Nature Reviews Cardiology, Published online: 02 January 2025; doi:10.1038/s41569-024-01110-1 In this Review, Dey and colleagues explore the pathobiology of coronary atherosclerotic plaques and perivascular adipose tissue, describe their phenotyping with computed tomography coronary angiography, and discuss potential future applications in clinical (..)
Researchers at Case Western Reserve University have identified a new target to treat atherosclerosis, a condition where plaque clogs arteries and causes major cardiac issues, including stroke and heart attack.
In a new study published in the European Heart Journal, researchers at Karolinska Institutet show that genetic traits influence the cellular composition of atherosclerotic plaques, which over time will affect the risk of such lesions for causing a stroke or heart attack.
In this 6-month randomized controlled study, twice-weekly HIIT reduced coronary plaque volume, increased aerobic fitness, and improved body composition in adults with stable heart disease, suggesting benefits for cardiovascular disease progression. Does this greater plaque presence put athletes at a greater risk of CVD events?
Aging is known to be a risk factor for the biological changes that create the dangerous buildup of plaque in arteries called atherosclerosis, and aging also induces a buildup of memory CD8 T cells, a type of immune cell, in mice and humans.
IntroductionCardiovascular disease (CVD) caused by atherosclerosis (AS) remains the leading cause of mortality in developed countries. Targeting this cell-cell interaction may offer new therapeutic avenues for managing atherosclerosis. These macrophages were associated with lipid transport, storage, and cell migration pathways.
Researchers have identified a new target to treat atherosclerosis, a condition where plaque clogs arteries and causes major cardiac issues, including stroke and heart attack.
The findings support that metals in the body are associated with the progression of plaque buildup in the arteries and potentially provide a new strategy for managing and preventing atherosclerosis.
Atherosclerosis, a disease characterized by the accumulation of lipids and inflammatory cells in the arterial wall, is a significant cause of cardiovascular events.
Notably, Apoe–/– mice expressing LL37 developed larger atheroma plaques than did control mice, and a positive correlation between plasma LL37 and oxidized phospholipid on apolipoprotein B (OxPL-apoB) levels was observed in individuals with cardiovascular disease.
Background Carotid artery atherosclerosis is a major cause of ischemic stroke, and ischemic stroke is the leading cause of morbidity and mortality worldwide. Unfortunately, the reason for the build-up of atherosclerosisplaque is unknown. However, such studies are rare and limited to animal experiments.
Atherosclerosis is, by definition, the abnormal retention of a cholesterol particle in the artery wall. Get Access The more particles you throw at your artery wall over a lifetime, the greater the chance one of those particles will be retained and form plaque. That is why addressing high cholesterol early in life is key.
Common examples of vascular disease are aneurysms (a dangerous bulge in an artery wall), atherosclerosis (plaque buildup in the… Source Vascular disease affects the body’s vast network of blood vessels, veins and arteries.
Although the entire vascular bed is constantly exposed to the same risk factors, atherosclerosis manifests a distinct intra-individual pattern in localization and progression within the arterial vascular bed.
PAD causes a narrowing of the peripheral arteries due to fatty plaque buildup (or atherosclerosis) which restricts blood flow to the extremities. PAD (Peripheral Artery Disease) is a common circulatory condition affecting more than 10 million Americans. This can lead to… Source
Researchers have discovered that the smooth muscle cells that line the arteries of people with atherosclerosis can change into new cell types and develop traits similar to cancer that worsen the disease.
Atherosclerosis (AS), a chronic inflammatory disease, remains a leading contributor to cardiovascular morbidity and mortality. This pathway is activated by cytoplasmic DNA from damaged cells, thereby triggering inflammation and accelerating plaque formation.
Introduction The progression of coronary atherosclerosis is an active and regulated process. The Wnt signaling pathway is thought to play an active role in the pathogenesis of several cardiovascular diseases; however, a better understanding of this system in atherosclerosis is yet to be unraveled.
Biomechanical forces, including vascular shear stress, cyclic stretching, and extracellular matrix stiffness, which influence mechanosensitive channels in the plasma membrane, determine cell function in atherosclerosis.
Background Inflammation is pivotal to the progression of atherosclerosis. Cholesterol crystals (CCs) that grow and enlarge within the plaque core can cause plaque rupture and trigger inflammation as they deposit into the atherosclerotic bed. Method Different dosages of colchicine mixed with cholesterol (0.05–5 mg/ml/g
Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardial infarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque. The pathologist may see a plaque that constitutes, for example, 50% of the cross-sectional area.
Doctor, do you have any investigation to know how much the total plaque burden is in my coronary artery? I recently read in Forbes Sunday health supplement, It says ,it is better to know the thickness of the cap covering the plaque. So, you want me to teach you the molecular biology of Atherosclerosis ,right ? Korean Circ J.
The sections were also used for immunohistochemistry with cell marker antibodies (to measure % plaque smooth muscle cells (SMC), macrophages (MF), and endothelial cells (EC)). to D: 30.7%), elevation in plaque MF (A: 16.7% to D: 22.5%), increase in plaque cell apoptosis (A: 5.2% to D:17.9%) and plaque EC (A:3.21% to D:1.48%).
Ipsilateral and contralateral carotid artery plaque features were compared, then the carotid artery plaque characteristics on the infarct side were correlated with the infarct pattern.Results:the mean age of subjects included was 68 years old, 79.6% of them were male. 0.15), larger wall area (0.50±0.19 0.23), all p values<0.05.
Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction and plaque formation. Under pro-inflammatory conditions, endothelial cells can undergo endothelial-to-mesenchymal transition (EndMT), contributing to atherosclerosis development.
You cannot eliminate the plaque entirely, but multiple clinical trials have shown plaque regression using high-intensity cholesterol-lowering treatments, which I have discussed previously. All of these parameters are important and need to be considered when evaluating plaque regression. REVERSAL Investigators.
The reason: They were accumulating plaque in their coronary arteries much earlier than their peers. You can’t have a heart attack if you don’t have plaque in your coronary arteries. And plaque in your coronary arteries is the result of exposure to risk factors over time. The answer: Risk Factors. The answer.
A high baseline level of high-sensitivity C-reactive protein (hsCRP) may indicate pan-coronary atherosclerosis and focal high-risk plaques in patients with a recent NSTEMI, according to a substudy of PROSPECT II published April 23.
The early detection of plaques by circulating biomarkers is highly clinically relevant to prevent the occurrence of major complications such as stroke or heart attacks. miRNA expression profiles of serum-derived EVs were obtained by small RNA sequencing and in plaque material simultaneously acquired from patients.
In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques.
The complex development of atherosclerosis manifests as intimal plaque which occurs in the presence or absence of traditional risk factors. Atherosclerotic coronary artery disease (CAD) is the causal pathological process driving most major adverse cardiovascular events (MACE) worldwide.
Atherosclerosis (AS) is a complex disease caused by multiple pathological factors threatening human health-the pathogenesis is yet to be fully elucidated.
BACKGROUND:Intensive lipid-lowering therapy may induce coronary atherosclerosis regression. A decrease in the percentage of unstable core (fibro-fatty+necrotic plaque; from 14.1 [7.9–22.3] Nevertheless, the factors underlying the effect of lipid-lowering therapy on disease regression remain poorly characterized. 10.6]; −6.6%;P<0.001)
CCR5, a chemokine receptor, has been associated with both immunosuppressive and inflammatory phenotypes, however, the possible role of CCR5 pertaining to MDSCs in the development of atherosclerosis has not been elucidated yet. Possibly this dysfunctionality contributes to the development and progression of CVD including atherosclerosis.
BackgroundPlaque progression (PP) is critical between subclinical atherosclerosis and plaque rupture. Journal of the American Heart Association, Ahead of Print. Small dense lowdensity lipoprotein cholesterol (sdLDLC) is considered as the most atherogenic lipoprotein.
Background Although the impact of hypertension on carotid intima-media thickness (IMT) and plaques has been well established, its association with femoral IMT and plaques has not been extensively examined. Ultrasonography was applied to assess the AS, including thickened IMT (TIMT) and plaque in the carotid and femoral arteries.
However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown. We explored the mechanism of METTL4 involvement in atherosclerosis usingMettl4Mac-KO-Apoe-/-andMettl4MUT-Apoe-/-mice and cell models, as well as bone marrow transplantation.
The goal of the PACMAN-AMI trial was to demonstrate the efficacy of early administration of alirocumab on plaque characteristics among patients undergoing percutaneous coronary intervention (PCI) for an acute myocardial infarction (AMI).
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content