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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Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Guilielmus H.J.M. Ellenbroek,Gerardus P.J. van Hout,Leo Timmers,Pieter A. Doevendans,Gerard Pasterkamp,Imo E. Hoefer +5 more
TL;DR: Assessment of three clinically relevant outcome modalities in a pig acute myocardial infarction model: infarct size in relation to area at risk (IS/AAR) staining, 3-dimensional transesophageal echocardiography (TEE) and admittance-based pressure-volume (PV) loops.
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Hidden in Heart Failure
TL;DR: The importance of identifying genetic, inflammatory and infiltrative causes of heart failure to enable patients to access tailored management strategies is emphasised.
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Different Roles of Resident and Non-resident Macrophages in Cardiac Fibrosis
Si-yuan Hu,Meng Feng Yang,Shu-min Huang,Sen-jie Zhong,Qian Zhang,Hai-Hua Ding,Xiajun Xiong,Zhixi Hu,Yi Ping Yang +8 more
TL;DR: It is believed that inhibiting the infiltration of cardiac non-resident macrophages and promoting the proliferation and activation of cardiac resident macrophage are the key to improving cardiac fibrosis and improving cardiac function.
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Interplay of pro-inflammatory cytokines, pro-inflammatory microparticles and oxidative stress and recurrent ventricular arrhythmias in elderly patients after coronary stent implantations.
TL;DR: It is suggested that the pro-inflammatory microparticles, pro- inflammatory cytokines and oxidative stress may simultaneously induce and aggravate recurrent VA in elderly patients after coronary stenting.
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Role and mechanism of the nod-like receptor family pyrin domain-containing 3 inflammasome in oral disease.
TL;DR: The initiation and activation of the NLRP3 inflammasome are associated with the pathogenesis and progression of several representative oral diseases, including periodontitis, oral lichen planus, dental pulp disease, and oral cavity squamous cell carcinoma.
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