Pathophysiological role of the AT2 receptor in cardiovascular remodeling after myocardial infarction in mice

2011 ◽  
Vol 59 (S 01) ◽  
Author(s):  
D Biermann ◽  
M Kirstein ◽  
H Treede ◽  
L Conradi ◽  
M Didié ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
At2 Receptor ◽  
Cardiovascular Remodeling ◽  
Pathophysiological Role

The Role of Uric Acid in the Acute Myocardial Infarction: A Narrative Review

Angiology ◽  
2021 ◽  
pp. 000331972110125
Author(s):  
Atalay Demiray ◽  
Baris Afsar ◽  
Adrian Covic ◽  
Masanari Kuwabara ◽  
Charles J. Ferro ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Uric Acid ◽  
Adverse Outcomes ◽  
Narrative Review ◽  
Background Information ◽  
Pathophysiological Role ◽  
Artery Disease ◽  
Pathologic Processes

Increased serum uric acid (SUA) levels have been associated with various pathologic processes such as increased oxidative stress, inflammation, and endothelial dysfunction. Thus, it is not surprising that increased SUA is associated with various adverse outcomes including cardiovascular (CV) diseases. Recent epidemiological evidence suggests that increased SUA may be related to acute myocardial infarction (AMI). Accumulating data also showed that elevated UA has pathophysiological role in the development of AMI. However, there are also studies showing that SUA is not related to the risk of AMI. In this narrative review, we summarized the recent literature data regarding SUA and AMI after providing some background information for the association between UA and coronary artery disease. Future studies will show whether decreasing SUA levels is beneficial for outcomes related to AMI and the optimum SUA levels for best outcomes in CV diseases.

Cardiac chymase: pathophysiological role and therapeutic potential of chymase inhibitors

2005 ◽  
Vol 83 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Sheila A Doggrell ◽  
Janet C Wanstall
Keyword(s):  
Myocardial Infarction ◽  
Mast Cells ◽  
Animal Models ◽  
Therapeutic Potential ◽  
Pressure Overload ◽  
Mrna Levels ◽  
Ang Ii ◽  
Pathophysiological Role ◽  
Orally Active

On release from cardiac mast cells, α-chymase converts angiotensin I (Ang I) to Ang II. In addition to Ang II formation, α-chymase is capable of activating TGF-β1 and IL-1β, forming endothelins consisting of 31 amino acids, degrading endothelin-1, altering lipid metabolism, and degrading the extracellular matrix. Under physiological conditions the role of chymase in the mast cells of the heart is uncertain. In pathological situations, chymase may be secreted and have important effects on the heart. Thus, in animal models of cardiomyopathy, pressure overload, and myocardial infarction, there are increases in both chymase mRNA levels and chymase activity in the heart. In human diseased heart homogenates, alterations in chymase activity have also been reported. These findings have raised the possibility that inhibition of chymase may have a role in the therapy of cardiac disease. The selective chymase inhibitors developed to date include TY-51076, SUN-C8257, BCEAB, NK320, and TEI-E548. These have yet to be tested in humans, but promising results have been obtained in animal models of myocardial infarction, cardiomyopathy, and tachycardia-induced heart failure. It seems likely that orally active inhibitors of chymase could have a place in the treatment of cardiac diseases where injury-induced mast cell degranulation contributes to the pathology.Key words: cardiac chymase, pathophysiological role, inhibition.

Origin and Pathophysiological Role of Increased Plasma Endothelin-1 in Patients with Acute Myocardial Infarction

Angiology ◽  
1995 ◽  
Vol 46 (7) ◽  
pp. 557-565 ◽  
Author(s):  
Koichi Setsuta ◽  
Yoshihiko Seino ◽  
Yoshifumi Tomita ◽  
Jun Nejima ◽  
Teruo Takano ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelin 1 ◽  
Pathophysiological Role

scholarly journals Pathophysiological role of mitochondria-actin interactions in mouse hearts after myocardial infarction

2019 ◽  
Vol 92 (0) ◽  
pp. 2-YIA-21
Author(s):  
Tomohiro Tanaka ◽  
Akiyuki Nishimura ◽  
Kakeru Shimoda ◽  
Tsukasa Shimauchi ◽  
Takashi Toyama ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Pathophysiological Role

Pathophysiological role of neutrophils in acute myocardial infarction

2013 ◽  
Vol 110 (09) ◽  
pp. 501-514 ◽  
Author(s):  
Federico Carbone ◽  
Alessio Nencioni ◽  
François Mach ◽  
Nicolas Vuilleumier ◽  
Fabrizio Montecucco
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Tissue Damage ◽  
Acute Coronary Syndromes ◽  
Immune Cell ◽  
Therapeutic Interventions ◽  
Pathophysiological Role ◽  
Inflammatory Processes ◽  
Coronary Syndromes

SummaryThe pathogenesis of acute myocardial infarction is known to be mediated by systemic, intraplaque and myocardial inflammatory processes. Among different immune cell subsets, compelling evidence now indicates a pivotal role for neutrophils in acute coronary syndromes. Neutrophils infiltrate coronary plaques and the infarcted myocardium and mediate tissue damage by releasing matrix-degrading enzymes and reactive oxygen species. In addition, neutrophils are also involved in post-infarction adverse cardiac remodelling and neointima formation after angioplasty. The promising results obtained in preclinical models with pharmacological approaches interfering with neutrophil recruitment or function have confirmed the pathophysiological relevance of these immune cells in acute coronary syndromes and prompted further studies of these therapeutic interventions. This narrative review will provide an update on the role of neutrophils in acute myocardial infarction and on the pharmacological means that were devised to prevent neutrophil-mediated tissue damage and to reduce post-ischaemic outcomes.

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