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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Aucubin Protects against Myocardial Infarction-Induced Cardiac Remodeling via nNOS/NO-Regulated Oxidative Stress
Zheng Yang,Qing-Qing Wu,Yang Xiao,Ming Xia Duan,Chen Liu,Yuan Yuan,Yan-Yan Meng,Hai Han Liao,Qi-Zhu Tang +8 more
TL;DR: Aucubin protects against cardiac remodeling post-MI through activation of the nNOS/NO pathway, which subsequently attenuates the ROS production, increases Trx preservation, and leads to inhibition of the ASK1/JNK pathway.
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Getting to the heart of intracellular glucocorticoid regeneration: 11β-HSD1 in the myocardium.
Gillian A. Gray,Christopher I. White,Raphael F.P. Castellan,Sara J. McSweeney,Karen E. Chapman +4 more
TL;DR: In this article, the authors reviewed the evidence for glucocorticoid metabolism by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in the heart and for a role of the enzyme in determining the myocardial growth and physiological function.
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Baicalin inhibits inflammation and attenuates myocardial ischaemic injury by aryl hydrocarbon receptor
Yiqiang Xue,Xiaorong Shui,Weiqing Su,Yuan He,Xinlin Lu,Yu Zhang,Guosen Yan,Shian Huang,Wei Lei,Can Chen +9 more
TL;DR: This study aimed to investigate the potential effect of baicalin on myocardial ischaemic injury through inhibition of inflammation by inactivating the aryl hydrocarbon receptor (AhR).
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Injectable Nanocomposite Implants Reduce ROS Accumulation and Improve Heart Function after Infarction
Malka Shilo,Hadas Oved,Lior Wertheim,Idan Gal,Nadav Noor,Ori Green,Ester-Sapir Baruch,Doron Shabat,Assaf Shapira,Tal Dvir +9 more
TL;DR: In this article, a new heart therapy comprised of cardiac implants encapsulated within an injectable extracellular matrix-gold nanoparticle composite hydrogel is reported, which is shown to absorb reactive oxygen species in vitro and in vivo in mice ischemia reperfusion model.
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Extracardiac-Lodged Mesenchymal Stromal Cells Propel an Inflammatory Response against Myocardial Infarction via Paracrine Effects:
Yi Peng,Wei Pan,Yali Ou,Weifang Xu,Sussannah Kaelber,Cesario V. Borlongan,Meiqin Sun,Guolong Yu +7 more
TL;DR: A novel hypothesis is raised that the therapeutic effects of MSC transplantation for acute MI depends not primarily on the grafted cells in infarct myocardium, but that MSCs migrating to and being lodged in the extracardiac organs, demonstrating good graft survival and persistence, may render the therapeutic results in MI.
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