The inflammatory response in myocardial injury, repair, and remodelling.
TLDR
Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies in patients with myocardial infarction.Abstract:
Myocardial infarction triggers an intense inflammatory response that is essential for cardiac repair, but which is also implicated in the pathogenesis of postinfarction remodelling and heart failure. Signals in the infarcted myocardium activate toll-like receptor signalling, while complement activation and generation of reactive oxygen species induce cytokine and chemokine upregulation. Leukocytes recruited to the infarcted area, remove dead cells and matrix debris by phagocytosis, while preparing the area for scar formation. Timely repression of the inflammatory response is critical for effective healing, and is followed by activation of myofibroblasts that secrete matrix proteins in the infarcted area. Members of the transforming growth factor β family are critically involved in suppression of inflammation and activation of a profibrotic programme. Translation of these concepts to the clinic requires an understanding of the pathophysiological complexity and heterogeneity of postinfarction remodelling in patients with myocardial infarction. Individuals with an overactive and prolonged postinfarction inflammatory response might exhibit left ventricular dilatation and systolic dysfunction and might benefit from targeted anti-IL-1 or anti-chemokine therapies, whereas patients with an exaggerated fibrogenic reaction can develop heart failure with preserved ejection fraction and might require inhibition of the Smad3 (mothers against decapentaplegic homolog 3) cascade. Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies.read more
Citations
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DissertationDOI
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Aircraft noise exposure induces pro-inflammatory vascular conditioning and amplifies vascular dysfunction and impairment of cardiac function after myocardial infarction
Michael Molitor,Maria Teresa Bayo Jimenez,Omar Hahad,Claudius Witzler,Stefanie Finger,Venkata Garlapati,S. Rajlic,Tanja Knopp,T. Bieler,M. Aluia,Johannes Wild,Jeremy Lagrange,Recha Blessing,Steffen Rapp,Andreas Schulz,Hartmut Kleinert,Susanne Karbach,Sebastian Steven,W. Ruf,Philipp S. Wild,Andreas Daiber,Thomas Münzel,Philip Wenzel +22 more
TL;DR: In this paper , a mouse model of myocardial infarction (MI) and in humans with incident MI was used to determine the mechanisms of cardiovascular dysfunction and inflammation induced by aircraft noise.
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TRIF/EGFR signalling mediates angiotensin-II-induced cardiac remodelling in mice
TL;DR: Cardiac TRIF was a potential therapeutic target for attenuating cardiac pathophysiological remodelling and partially explained the molecular mechanism of Ang II-induced cardiac inflammation, fibrosis, hypertrophy and dysfunction in mice.
Journal ArticleDOI
Immunity and inflammation in cardiovascular disorders
TL;DR: A collection on the role of the immune system and inflammation in Cardiovascular Disease (CVD) has been published by BMC Cardiovascular Disorders (BMC-CD) as discussed by the authors .
Book ChapterDOI
Cardiovascular translational biomarkers: translational aspects of hypertension, atherosclerosis, and heart failure in drug development in the digital era
TL;DR: In this chapter, three indications (hypertension, atherosclerosis, and heart failure) are profiled against the use of major biomarkers in drug development, and derived learnings are applied to a fourth one in the form of a case study involving atrial fibrillation.
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