placeholder
and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Proceed order?

Export
Filter
Language
Year
  • 1
    Language: English
    In: Journal of the American College of Cardiology, 2017-10-31, Vol.70 (18), p.2278-2289
    Description: Inflammatory pathways drive atherogenesis and link conventional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1β) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients.
    Subject(s): Atherosclerosis - blood ; Animals ; Atherosclerosis - drug therapy ; Humans ; Anti-Inflammatory Agents - administration & dosage ; Biomarkers - blood ; Drug Delivery Systems - trends ; Anti-Inflammatory Agents - metabolism ; Drug Delivery Systems - methods ; Interleukin-1beta - antagonists & inhibitors ; Interleukin-1beta - blood ; Medical colleges ; Interleukins ; Cardiac patients ; Therapeutics ; Atherosclerosis ; Health aspects ; Coronary heart disease ; Cardiovascular agents ; Homeopathy ; Materia medica and therapeutics ; Index Medicus ; Abridged Index Medicus
    ISSN: 0735-1097
    E-ISSN: 1558-3597
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Article
    Article
    2013
    ISSN: 0028-4793 
    Language: English
    In: The New England journal of medicine, 2013-05-23, Vol.368 (21), p.2004-2013
    Description: The notion that heart attacks develop from coronary-artery stenosis is an oversimplification of a process involving lipid metabolism, inflammation, macrophage activation, collagen breakdown, and plaque rupture. These insights are leading to new ideas for treatment and prevention. Atherosclerotic lesions in humans typically form over the course of years to decades, one of the longest incubation periods among human diseases. Despite the chronicity of atherosclerosis, thrombotic complications — the most dreaded clinical consequences of this disease — occur suddenly, and often without warning. Our familiarity with the disease has generally led us to accept this apparent paradox without wonder. What mechanisms explain the abrupt transition from stable ischemic heart disease or asymptomatic atherosclerosis to acute coronary syndromes? This review examines our current understanding of the mechanisms underlying these syndromes. According to the traditional view, progressive stenosis narrows the . . .
    Subject(s): Cardiology. Vascular system ; Heart ; General aspects ; Biological and medical sciences ; Myocarditis. Cardiomyopathies ; Medical sciences ; Coronary heart disease ; Plaque, Atherosclerotic - complications ; Acute Coronary Syndrome - therapy ; Plaque, Atherosclerotic - pathology ; Humans ; Acute Coronary Syndrome - etiology ; Plaque, Atherosclerotic - physiopathology ; Prevention ; Care and treatment ; Research ; Acute coronary syndrome ; Cell activation ; Heart attacks ; Coronary vessels ; Collagen ; Coronary artery ; Stenosis ; Cardiovascular disease ; Lipid metabolism ; Macrophages ; Angina pectoris ; Index Medicus ; Abridged Index Medicus
    ISSN: 0028-4793
    E-ISSN: 1533-4406
    Source: Single Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Article
    Article
    2013
    ISSN: 0021-9738 
    Language: English
    In: The Journal of clinical investigation, 2013-08, Vol.123 (8), p.3201-3203
    Description: The core of an atheromatous plaque contains lipids, macrophages, and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from the blood. Rupture of the fibrous cap causes most fatal myocardial infarctions. Interstitial collagen confers tensile strength on the cap, as it does in skin and tendons. In 1994, Peter Libby and colleagues demonstrated overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabilization of these lesions.
    Subject(s): Plaque, Atherosclerotic - complications ; Atherosclerosis - enzymology ; Animals ; Plaque, Atherosclerotic - enzymology ; Humans ; Atherosclerosis - complications ; Collagenases - physiology ; Myocardial Infarction - etiology ; Myocardial Infarction - enzymology ; Collagenases ; Physiological aspects ; Research ; Gene expression ; Atherosclerotic plaque ; Enzymes ; Rabbits ; Wound healing ; Heart attacks ; Lipids ; Smooth muscle ; Biology ; Experiments ; Thrombosis ; Biomechanics ; Hypotheses ; Collagen ; Atherosclerosis ; Acute coronary syndromes ; Index Medicus ; Abridged Index Medicus ; Hindsight
    ISSN: 0021-9738
    E-ISSN: 1558-8238
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Article
    Article
    2020
    ISSN: 0028-0836 
    Language: English
    In: Nature (London), 2020-05, Vol.581 (7808), p.263-264
    Subject(s): Prevalence ; Dysbiosis ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Humans ; Gastrointestinal Microbiome ; Overweight persons ; Microbiota (Symbiotic organisms) ; Analysis ; Dosage and administration ; Drug therapy ; Health aspects ; Statins ; Microorganisms
    ISSN: 0028-0836
    E-ISSN: 1476-4687
    Source: Alma/SFX Local Collection
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: The American journal of medicine, 2008, Vol.121 (10), p.S21-S31
    Description: Abstract Rheumatoid arthritis (RA) is associated with excess morbidity and mortality from myocardial infarction and allied disorders. A large body of evidence supports the involvement of common proinflammatory cytokines in the development and progression of both RA and atherosclerosis. The destructive proinflammatory cascade and effector mechanisms implicated in RA resemble the chronic inflammatory processes that drive the development of atherosclerosis in general. Proinflammatory cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor-α produced within locally affected joints in RA may promote both traditional (e.g., dyslipidemia, insulin resistance) and nontraditional (e.g., oxidative stress) systemic cardiovascular risk factors. Expression of proinflammatory cytokines and inflammatory mediators influences all stages of atherosclerosis development, from early atheroma formation to thrombus development responsible for events such as myocardial infarction. Appreciation of the inflammatory process shared by RA and atherosclerosis should heighten the recognition of this morbid association and lead to better recognition and management of cardiovascular risk in patients with rheumatologic diseases.
    Subject(s): Internal Medicine ; Cardiovascular disease ; Inflammation ; Rheumatoid arthritis ; Atherosclerosis ; Cardiology. Vascular system ; Biological and medical sciences ; General aspects ; Medical sciences ; Atherosclerosis (general aspects, experimental research) ; Blood and lymphatic vessels ; United States - epidemiology ; Arthritis, Rheumatoid - blood ; Humans ; Risk Factors ; Inflammation - immunology ; Biomarkers - blood ; Arthritis, Rheumatoid - complications ; Atherosclerosis - epidemiology ; Inflammation - blood ; Morbidity ; Atherosclerosis - blood ; Atherosclerosis - etiology ; Inflammation - complications ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Arthritis, Rheumatoid - immunology ; Immunity, Cellular ; Cytokines - blood ; Endothelium, Vascular - immunology ; Index Medicus ; Abridged Index Medicus
    ISSN: 0002-9343
    E-ISSN: 1555-7162
    Source: ScienceDirect Journals
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Article
    Article
    2002
    ISSN: 0028-0836 
    Language: English
    In: Nature (London), 2002-12-19, Vol.420 (6917), p.868-874
    Description: Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.
    Subject(s): Cardiology. Vascular system ; Biological and medical sciences ; Medical sciences ; Atherosclerosis (general aspects, experimental research) ; Blood and lymphatic vessels ; Arteriosclerosis - etiology ; Chemotaxis, Leukocyte ; Arteriosclerosis - therapy ; Inflammation - pathology ; Disease Susceptibility ; Tunica Intima - immunology ; Humans ; Risk ; Inflammation - immunology ; Leukocytes - immunology ; Inflammation - complications ; Inflammation - therapy ; Animals ; Tunica Intima - pathology ; Arteriosclerosis - immunology ; Arteriosclerosis - pathology ; Index Medicus
    ISSN: 0028-0836
    E-ISSN: 1476-4687
    Source: Nature Journal Archive
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Journal of the American College of Cardiology, 2018-07-03, Vol.72 (1), p.58-61
    Description: [Display omitted]
    Subject(s): CD31 ; peptides ; macrophages ; drug discovery ; intramural hematoma ; aortic dissection ; Macrophages ; Humans ; Aortic Aneurysm ; Aneurysm, Dissecting ; Aortic Diseases
    ISSN: 0735-1097
    E-ISSN: 1558-3597
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Article
    Article
    2019
    ISSN: 1050-1738 
    Language: English
    In: Trends in cardiovascular medicine, 2019-11, Vol.29 (8), p.473-475
    Description: Inflammation drives the formation, evolution, and complication of atherosclerotic plaques. Yet, we have not yet captured the culprits who light the fire that burns within the atherosclerotic plaque. The arsonist remains at large. A rigorous analysis exculpates many of the usual suspects. Low-density lipoprotein (LDL) itself engenders little inflammation. Clinical trials do not support an actionable role of oxidized LDL in atherothrombosis. In contrast, triglyceride-rich lipoproteins do promote inflammation, and provide a promising target for intervention. Obese adipose tissue —especially visceral or ectopic lipid deposits —also incite inflammation. A newly recognized cardiovascular risk factor, clonal hematopoiesis provides a novel link between inflammatory pathways and atherosclerotic risk. Despite this progress, the jury is still out on who lit the plaque afire. The rigorous observer must still consider this an unsolved act of arson. We remain in “hot” pursuit of the causal culprit, the arsonist, and accomplices who set the artery wall ablaze.
    Subject(s): Triglyceride-rich lipoproteins ; Inflammation ; Endotoxin ; Clonal hematopoiesis ; Microbiome ; Firesetting Behavior ; Humans ; Atherosclerosis ; Infections ; Plaque, Atherosclerotic ; Arteries ; Lipoproteins, LDL ; Arson ; Triglycerides ; Blood lipids ; Atherosclerotic plaque ; Low density lipoproteins ; Cardiovascular agents ; Index Medicus
    ISSN: 1050-1738
    E-ISSN: 1873-2615
    Source: ProQuest Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Article
    Article
    2020
    ISSN: 0195-668X 
    Language: English
    In: European heart journal, 2020-09-01, Vol.41 (32), p.3038-3044
    Description: The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.
    Subject(s): Thrombosis - physiopathology ; Pandemics ; Cytokines - metabolism ; Oxidative Stress ; Humans ; Endothelium, Vascular - physiopathology ; COVID-19 ; SARS-CoV-2 ; Thrombosis - metabolism ; Coronavirus Infections - epidemiology ; Pneumonia, Viral - epidemiology ; Thrombosis - etiology ; Pneumonia, Viral - complications ; Betacoronavirus ; Coronavirus Infections - complications ; Index Medicus ; Viewpoint ; Cytokine ; MED00200 ; Inflammation ; Microvasculature ; AcademicSubjects ; Thrombosis ; Endothelium
    ISSN: 0195-668X
    E-ISSN: 1522-9645
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Article
    Article
    2006
    ISSN: 0002-9149 
    Language: English
    In: The American journal of cardiology, 2006, Vol.98 (12), p.S3-S9
    Description: The concept of the vulnerable plaque has generated much interest and stimulated a quest to develop diagnostic modalities to identify potentially unstable atherosclerotic plaques. However, accumulating clinical data now suggest that multiple vulnerable plaques coexist in a single coronary tree and that inflammation is a critical determinant of the stability of plaques. Inflammatory mediators, such as cytokines, can influence several biologic processes that regulate stability of the plaque’s fibrous cap and its resistance to rupture. Thus, the quest for strategies to identify and target treatment to a single culprit lesion seriously underestimates the complexity of the clinical biology of thrombosis in atherosclerotic arteries. For the optimum management of our patients, we must now also consider the vulnerable artery, the vulnerable arterial bed, and ultimately, the vulnerable patient. Treatment of vulnerable patients should include measures to stabilize plaques and to lessen the thrombotic consequences of plaque disruptions.
    Subject(s): Cardiology. Vascular system ; Heart ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Medical sciences ; Coronary heart disease ; Blood and lymphatic vessels ; Myocardial Infarction - prevention & control ; Coronary Artery Disease - physiopathology ; Myocardial Infarction - etiology ; Coronary Artery Disease - complications ; Humans ; Coronary Artery Disease - prevention & control ; Atherosclerosis ; Index Medicus ; Abridged Index Medicus
    ISSN: 0002-9149
    E-ISSN: 1879-1913
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...