Methylglyoxal and glyoxalase I in atherosclerosis

2014 ◽  
Vol 42 (2) ◽  
pp. 443-449 ◽  
Author(s):  
Nordin M.J. Hanssen ◽  
Coen D.A. Stehouwer ◽  
Casper G. Schalkwijk
Keyword(s):  
Metabolic Activity ◽  
Causes Of Death ◽  
Plaque Rupture ◽  
Glyoxalase I ◽  
Atherosclerotic Plaques ◽  
Glycation End Products ◽  
Plaque Phenotype ◽  
Atherosclerotic Plaque Rupture ◽  
Progression Of Atherosclerosis ◽  
High Metabolic Activity

Cardiovascular disease, caused predominantly by atherosclerotic plaque rupture, remains one of the leading causes of death. However, the mechanism of plaque rupture remains largely unknown. Recent studies have linked high metabolic activity in inflamed atherosclerotic plaques to the development of plaque rupture. AGEs (advanced glycation end-products) are known to be formed as a result of high metabolic activity and are higher in rupture-prone than stable plaques. Furthermore, AGEs seem to be more than mere markers of metabolic activity, as recent studies have elucidated that AGEs and their major precursor, MG (methylglyoxal), may have an important role in the progression of atherosclerosis and plaque rupture. MG can be detoxified by Glo1 (glyoxalase I), thereby preventing the accumulation of MG and MG-derived AGEs. In the present review, data concerning MG, Glo1 and AGEs in the context of plaque phenotype are discussed.

scholarly journals Clinical Implications of IL-32, IL-34 and IL-37 in Atherosclerosis: Speculative Role in Cardiovascular Manifestations of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Ching Chee Law ◽  
Rajesh Puranik ◽  
Jingchun Fan ◽  
Jian Fei ◽  
Brett D. Hambly ◽  
...  
Keyword(s):  
Plaque Rupture ◽  
Chronic Inflammatory Disease ◽  
Atherosclerotic Plaques ◽  
The Novel ◽  
Unstable Plaque ◽  
Innate And Adaptive Immunity ◽  
Coronary Syndrome ◽  
Plaque Phenotype ◽  
Unstable Plaques ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis, which is a primary cause of cardiovascular disease (CVD) deaths around the world, is a chronic inflammatory disease that is characterised by the accumulation of lipid plaques in the arterial wall, triggering inflammation that is regulated by cytokines/chemokines that mediate innate and adaptive immunity. This review focuses on IL-32, -34 and -37 in the stable vs. unstable plaques from atherosclerotic patients. Dysregulation of the novel cytokines IL-32, -34 and -37 has been discovered in atherosclerotic plaques. IL-32 and -34 are pro-atherogenic and associated with an unstable plaque phenotype; whereas IL-37 is anti-atherogenic and maintains plaque stability. It is speculated that these cytokines may contribute to the explanation for the increased occurrence of atherosclerotic plaque rupture seen in patients with COVID-19 infection. Understanding the roles of these cytokines in atherogenesis may provide future therapeutic perspectives, both in the management of unstable plaque and acute coronary syndrome, and may contribute to our understanding of the COVID-19 cytokine storm.

INTRAVASCULAR ULTRASOUND PALPOGRAPHY: A NEW METHOD FOR THE DETECTION OF THE VULNERABLE PLAQUE

2006 ◽  
Vol 06 (01) ◽  
pp. 35-38
Author(s):  
FRANCESCO SAIA ◽  
JOHANNES A. SCHAAR ◽  
FRITS MASTIK ◽  
CHRIS L. DE KORTE ◽  
SAMANTHA CORNACCHIA ◽  
...  
Keyword(s):  
Intravascular Ultrasound ◽  
Plaque Rupture ◽  
Coronary Thrombosis ◽  
Local Strain ◽  
Coronary Event ◽  
Diagnostic Methods ◽  
Atherosclerotic Plaques ◽  
Clinical Markers ◽  
Coronary Syndromes ◽  
Atherosclerotic Plaque Rupture

Acute coronary syndromes originate from atherosclerotic plaque rupture and subsequent developement of coronary thrombosis. Available screening and diagnostic methods are insufficient to identify the atherosclerotic plaques that will rupture and precipitate the coronary event. We developed a new intracoronary diagnostic method based on intravascular ultrasound (IVUS) examination to evaluate the local mechanical properties of atherosclerotic plaques namely IVUS-elastography/palpography. The relationships between local strain, histological features of vulnerability, clinical presentation, and clinical markers of instability were assessed.

Cyclic Bending of Coronary Plaques Leads to Much Higher Stress Variations: A Major Factor Contributing to Plaque Rupture Risk

2007 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Shunichi Kobayashi ◽  
Gregorio A. Sicard ◽  
...  
Keyword(s):  
Plaque Rupture ◽  
Strain Analysis ◽  
Atherosclerotic Plaques ◽  
Rupture Risk ◽  
Cyclic Bending ◽  
Clinical Events ◽  
Stenosis Severity ◽  
Atherosclerotic Plaque Rupture ◽  
Component Models ◽  
Stress Variations

Mechanical forces play an important role in the complicated process of atherosclerotic plaque rupture which often leads to serious clinical events such as stroke and heart attack [4]. Factors causing the vulnerable plaque cap to fracture are important clinically [2–7]. It is known that coronary plaques are more likely to rupture compared to carotid plaques under comparable conditions (such as stenosis severity at about 50% by diameter). One possible reason is that coronary arteries are under cyclic bending caused by heart motions and compressions. We hypothesize that cyclic bending of coronary atherosclerotic plaques may be a major contributor to critical stress variations in the plaque leading to increased plaque rupture risk. We have developed MRI-based 3D multi-component models with fluid-structure interactions (FSI) in order to perform flow and stress/strain analysis for atherosclerotic plaques and identify possible mechanical and morphological indices for accurate plaque vulnerability assessment [6–7].

scholarly journals BIOMARKERS IDENTIFICATION AND THERAPY TARGET IN MACROPHAGE OF ATHEROSCLEROSIS: SYSTEMATIC REVIEW

2021 ◽  
pp. 30-39
Author(s):  
NENG FISHERI KURNIATI ◽  
HUBBI NASHRULLAH MUHAMMAD ◽  
GAYUK KALIH PRASESTI
Keyword(s):  
Systematic Review ◽  
Signaling Pathway ◽  
Plaque Rupture ◽  
Atherosclerotic Plaques ◽  
Molecular Signaling ◽  
Inclusion Criteria ◽  
Therapy Targets ◽  
Research Procedure ◽  
Therapy Target ◽  
Progression Of Atherosclerosis

Macrophages are known to play an important role in the initiation and progression of atherosclerosis; however, the molecular signaling pathways in macrophages that are responsible for plaque rupture have not been fully identified. This study aims to identify biomarkers and therapy targets in macrophages in atherosclerotic conditions by systematic review. Research procedure of systematic reviews using the PRISMA protocol. The search engine used in this study is PubMed, with the keywords ([macrophage] AND atherosclerosis) AND (signaling pathway OR signaling pathway), the reference application used is Zotero to screen clinical articles. There were 689 articles identified and 11 clinical articles in inclusion criteria were obtained. The identification resulted in 30 biomarkers associated with macrophages in atherosclerotic conditions. The proposed biomarkers of atherosclerosis are interleukin (IL)-1β and IL-18. The proposed potential therapy targets for atherosclerosis are LOX-1 and schematic images of biomarkers in atherosclerotic plaques.

scholarly journals From Mitochondria to Atherosclerosis: The Inflammation Path

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 258
Author(s):  
Juan M. Suárez-Rivero ◽  
Carmen J. Pastor-Maldonado ◽  
Suleva Povea-Cabello ◽  
Mónica Álvarez-Córdoba ◽  
Irene Villalón-García ◽  
...  
Keyword(s):  
Plaque Rupture ◽  
Mitochondrial Dynamics ◽  
Chronic Inflammatory Disease ◽  
Mitochondrial Dysfunctions ◽  
Innate Defense ◽  
Arterial Lumen ◽  
Unstable Atherosclerotic Plaque ◽  
Atherosclerotic Plaque Rupture ◽  
Progression Of Atherosclerosis

Inflammation is a key process in metazoan organisms due to its relevance for innate defense against infections and tissue damage. However, inflammation is also implicated in pathological processes such as atherosclerosis. Atherosclerosis is a chronic inflammatory disease of the arterial wall where unstable atherosclerotic plaque rupture causing platelet aggregation and thrombosis may compromise the arterial lumen, leading to acute or chronic ischemic syndromes. In this review, we will focus on the role of mitochondria in atherosclerosis while keeping inflammation as a link. Mitochondria are the main source of cellular energy. Under stress, mitochondria are also capable of controlling inflammation through the production of reactive oxygen species (ROS) and the release of mitochondrial components, such as mitochondrial DNA (mtDNA), into the cytoplasm or into the extracellular matrix, where they act as danger signals when recognized by innate immune receptors. Primary or secondary mitochondrial dysfunctions are associated with the initiation and progression of atherosclerosis by elevating the production of ROS, altering mitochondrial dynamics and energy supply, as well as promoting inflammation. Knowing and understanding the pathways behind mitochondrial-based inflammation in atheroma progression is essential to discovering alternative or complementary treatments.

Ultrastructural aspects of gymnosperms reproductive organs tissues due to their functional condition

1978 ◽  
Vol 36 (2) ◽  
pp. 440-441
Author(s):  
G. M. Kozubov
Keyword(s):  
Metabolic Activity ◽  
Functional Condition ◽  
Reproductive Organs ◽  
Considerable Change ◽  
Complicated Structure ◽  
Tetrad Stage ◽  
Ubisch Bodies ◽  
Similar Organization ◽  
Female Reproductive Organs ◽  
High Metabolic Activity

The ultrastructure of reproductive organs of pine, spruce, larch and ginkgo was investigated. It was found that the male reproductive organs possess similar organization. The most considerable change in the ultrastructure of the microsporocytes occur in meiosis. Sporoderm is being laid at the late tetrad stage. The cells of the male gameto-phyte are distinguished according to the metabolic activity of the or- ganells. They are most weakly developed in the spermiogenic cell. Ta-petum of the gymnosperms is of the periplasmodic - secretorial type. The Ubisch bodies which possess similar structure in the types investigated but are specific in details in different species are produced in tapetum.Parietal and subepidermal layers are distinguished for their high metabolic activity and are capable of the autonomous photosynthesis. Female reproductive organs differ more greatly in their struture and have the most complicated structure in primitive groups. On the first stages of their formation the inner cells of nucellus are transformed into the nucellar tapetum in which the structures similar to the Ubisch bodies taking part in the formation of the sporoderm of female gametophyte have been found.

Deficiency of endothelial CD40 induces a stable plaque phenotype and limits inflammatory cell recruitment to atherosclerotic lesions in mice

2021 ◽  
Author(s):  
Mark Colin Gissler ◽  
Philipp Scherrer ◽  
Nathaly Anto Michel ◽  
Jan Pennig ◽  
Natalie Hoppe ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Inflammatory Cell ◽  
Leukocyte Adhesion ◽  
Critical Role ◽  
Atherosclerotic Lesion ◽  
Intercellular Adhesion Molecule ◽  
Atherosclerotic Plaques ◽  
Chow Diet ◽  
Stable Plaque ◽  
Plaque Phenotype

Objectives: The co-stimulatory CD40L-CD40 dyad exerts a critical role in atherosclerosis by modulating leukocyte accumulation into developing atherosclerotic plaques. The requirement for cell-type specific expression of both molecules, however, remains elusive. Here, we evaluate the contribution of CD40 expressed on endothelial cells (ECs) in a mouse model of atherosclerosis. Approach & Results: Atherosclerotic plaques of Apolipoprotein E deficient (Apoe-/-) mice and humans displayed increased expression of CD40 on ECs compared to controls. To interrogate the role of CD40 on ECs in atherosclerosis, we induced EC-specific (BmxCreERT2-driven) deficiency of CD40 in Apoe-/- mice. After feeding a chow diet for 25 weeks, EC-specific deletion of CD40 (iEC-CD40) ameliorated plaque lipid deposition and lesional macrophage accumulation but increased intimal smooth muscle cell and collagen content, while atherosclerotic lesion size did not change. Leukocyte adhesion to the vessel wall was impaired in iEC-CD40-deficient mice as demonstrated by intravital microscopy. In accord, expression of vascular adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 in the vascular endothelium declined after deletion of CD40. In vitro, antibody-mediated inhibition of human endothelial CD40 significantly abated monocyte adhesion on ECs. Conclusions: Endothelial deficiency of CD40 in mice promotes structural features associated with a stable plaque phenotype in humans and decreases leukocyte adhesion. These results suggest that endothelial-expressed CD40 contributes to inflammatory cell migration and consecutive plaque formation in atherogenesis.

Ferrite-encapsulated nanoparticles with stable photothermal performance for multimodal imaging-guided atherosclerotic plaque neovascularization therapy

2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Multimodal Imaging ◽  
Plaque Rupture ◽  
Pathological Angiogenesis ◽  
Atherosclerotic Plaque Rupture ◽  
Encapsulated Nanoparticles

Pathological angiogenesis is a critical contributor to atherosclerotic plaque rupture. However, there are few effective theranostic strategies to stabilize plaques by suppressing neovascularization. A polymeric nanosystem using 3 nm manganese...

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