scholarly journals Research Progress on the Relationship between Atherosclerosis and Inflammation

Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 80 ◽  
Author(s):  
Yuhua Zhu ◽  
Xuemei Xian ◽  
Zhenzhen Wang ◽  
Yingchao Bi ◽  
Quangang Chen ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Plaque Rupture ◽  
Chronic Inflammatory Disease ◽  
Research Progress ◽  
Bioactive Lipids ◽  
Inflammatory Signaling ◽  
Vascular Stenosis ◽  
Unstable Atherosclerotic Plaque ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis is a chronic inflammatory disease; unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. Atherosclerosis-related inflammation is mediated by proinflammatory cytokines, inflammatory signaling pathways, bioactive lipids, and adhesion molecules. This review discusses the effects of inflammation and the systemic inflammatory signaling pathway on atherosclerosis, the role of related signaling pathways in inflammation, the formation of atherosclerosis plaques, and the prospects of treating atherosclerosis by inhibiting inflammation.

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.

scholarly journals Emerging science on whole grain intake and inflammation

2020 ◽  
Vol 78 (Supplement_1) ◽  
pp. 21-28
Author(s):  
Shengmin Sang ◽  
Emmanuel Idehen ◽  
Yantao Zhao ◽  
YiFang Chu
Keyword(s):  
Gut Microbiota ◽  
Signaling Pathways ◽  
Subclinical Inflammation ◽  
Whole Grain ◽  
Biological Mechanisms ◽  
Inflammatory Signaling ◽  
Bioactive Substances ◽  
The Relationship ◽  
Reduced Risk

Abstract Although the biological mechanisms surrounding the widely reported association between whole grain (WG) consumption and reduced risk of several diseases are not fully understood, there is growing evidence suggesting that inflammation may be an essential mediator in this multifaceted process. It also appears that several mechanisms influence the modulatory actions of WGs on inflammation, including the effect of fiber, phytochemicals, and their microbial-derived metabolites. While some of these effects are direct, others involve gut microbiota, which transform important bioactive substances into more useful metabolites that moderate inflammatory signaling pathways. This review evaluates emerging evidence of the relationship between WGs and their effects on markers of subclinical inflammation, and highlights the role of fiber, unique WG phytochemicals, and gut microbiota on the anti-inflammatory effects of WG intake.

Comparison of two murine models of thrombosis induced by atherosclerotic plaque injury

2011 ◽  
Vol 105 (S 06) ◽  
pp. S3-S12 ◽  
Author(s):  
Béatrice Hechler ◽  
Christian Gachet
Keyword(s):  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Vascular Lesions ◽  
Murine Models ◽  
Atherosclerotic Lesions ◽  
Human Pathology ◽  
Rupture Model ◽  
Atherosclerotic Plaque Rupture ◽  
Collagen Receptor

SummaryArterial thrombosis occurs at sites of erosion or rupture of atherosclerotic vascular lesions. To better study the pathophysiology of this complex phenomenon, there is a need for animal models of localised thrombosis at sites of atherosclerotic lesions with closer resemblance to the human pathology as compared to commonly used thrombosis models in healthy vessels. In the present study, we describe and compare a new model of thrombosis induced by atherosclerotic plaque rupture in the carotid artery from ApoE-/- mice using a suture needle to a milder model of ultrasound-induced plaque injury. Needle injury induces atherosclerotic plaque rupture with exposure of plaque material and formation of a thrombus that is larger, nearly occlusive and more stable as compared to that formed by application of ultrasounds. These two models have common features such as the concomitant involvement of platelet activation, thrombin generation and fibrin formation, which translates into sensitivity toward both antiplatelet drugs and anticoagulants. On the other hand, they display differences with respect to the role of the platelet collagen receptor GPVI, the plaque rupture model being less sensitive to its inhibition as compared to the ultrasound-induced injury, which may be related to the amount of thrombin generated. These models represent an improvement as compared to models in healthy vessels and may help identify specific plaque triggers of thrombosis. They should therefore be useful to evaluate new antithrombotic targets.

Role of physical exercise on hepatic insulin, glucocorticoid and inflammatory signaling pathways in an animal model of non-alcoholic steatohepatitis

Life Sciences ◽  
2015 ◽  
Vol 123 ◽  
pp. 51-60 ◽  
Author(s):  
E. Passos ◽  
C.D. Pereira ◽  
I.O. Gonçalves ◽  
S. Rocha-Rodrigues ◽  
N. Silva ◽  
...  
Keyword(s):  
Animal Model ◽  
Physical Exercise ◽  
Signaling Pathways ◽  
Inflammatory Signaling ◽  
Alcoholic Steatohepatitis

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.

scholarly journals Current Research Progress of the Role of LncRNA LEF1-AS1 in a Variety of Tumors

2021 ◽  
Vol 9 ◽  
Author(s):  
Qingyuan Zheng ◽  
Xiao Yu ◽  
Menggang Zhang ◽  
Shuijun Zhang ◽  
Wenzhi Guo ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Target Genes ◽  
Malignant Tumors ◽  
Underlying Mechanism ◽  
Research Progress ◽  
Diagnosis And Prognosis ◽  
Binding Factor ◽  
Non Coding Rnas ◽  
The Relationship

Long non-coding RNAs (lncRNA), as key regulators of cell proliferation and death, are involved in the regulation of various processes in the nucleus and cytoplasm, involving biological developmental processes in the fields of immunology, neurobiology, cancer, and stress. There is great scientific interest in exploring the relationship between lncRNA and tumors. Many researches revealed that lymph enhancer-binding factor 1-antisense RNA 1 (LEF1-AS1), a recently discovered lncRNA, is downregulated in myeloid malignancy, acting mainly as a tumor suppressor, while it is highly expressed and carcinogenic in glioblastoma (GBM), lung cancer, hepatocellular carcinoma (HCC), osteosarcoma, colorectal cancer (CRC), oral squamous cell carcinoma (OSCC), prostatic carcinoma, retinoblastoma, and other malignant tumors. Furthermore, abnormal LEF1-AS1 expression was associated with tumorigenesis, development, survival, and prognosis via the regulation of target genes and signaling pathways. This review summarizes the existing data on the expression, functions, underlying mechanism, relevant signaling pathways, and clinical significance of LEF1-AS1 in cancer. It is concluded that LEF1-AS1 can serve as a novel biomarker for the diagnosis and prognosis of various tumors, thus deserves further attention in the future.

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