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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Differences in Stem Cell Processing Lead to Distinct Secretomes Secretion—Implications for Differential Results of Previous Clinical Trials of Stem Cell Therapy for Myocardial Infarction
Bernhard Wernly,Inês Fonseca Gonçalves,Attila Kiss,Vera Paar,Tobias Mösenlechner,Michael Leisch,D. Santer,Lucas Motloch,Klaus Ulrich Klein,Eva Verena Tretter,Daniel Kretzschmar,Bruno K. Podesser,Christian Jung,Uta C. Hoppe,Michael Lichtenauer +14 more
TL;DR: The REPAIR-AMI secretome significantly enhances proangiogenic chemokine secretion, angiogenesis, cell migration, and cardioprotective signaling pathways and might open a new therapeutic concept for improving patient outcome.
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Loss of Camk2n1 aggravates cardiac remodeling and malignant ventricular arrhythmia after myocardial infarction in mice via NLRP3 inflammasome activation.
Zhixing Wei,Yudong Fei,Qian Wang,Jianwen Hou,Xingxing Cai,Yuli Yang,Tai-Zhong Chen,Quanfu Xu,Yue-Peng Wang,Yi-Gang Li +9 more
TL;DR: In this paper, the role of CaMKII inhibitor 1 (Camk2n1) on the process of arrhythmia substrate generation following myocardial infarction (MI) was investigated.
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5-Methoxytryptophan attenuates postinfarct cardiac injury by controlling oxidative stress and immune activation.
Wan-Tseng Hsu,Ya-Hsuan Tseng,Hsiang-Yiang Jui,Chen-Chin Kuo,Kenneth K. Wu,Chii-Ming Lee,Chii-Ming Lee +6 more
TL;DR: In this article, the effect of exogenous 5-MTP administration on rescuing post-MI cardiac injury was evaluated using echocardiography, triphenyltetrazolium chloride staining, and Masson trichrome staining.
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Association of Myocardial Injury With Serum Procalcitonin Levels in Patients With ST-Elevation Myocardial Infarction.
Martin Reindl,Christina Tiller,Magdalena Holzknecht,Ivan Lechner,Benjamin Henninger,Agnes Mayr,Christoph Brenner,Gert Klug,Axel Bauer,Bernhard Metzler,Sebastian J. Reinstadler +10 more
TL;DR: These data highlight the clinical potential of procalcitonin to identify concomitant infection and to guide antibiotic treatments for patients with ST-elevation myocardial infarction; however, randomized trials are needed to evaluate the clinical benefit of a procalCitonin-guided strategy.
Journal ArticleDOI
The tumor suppressor RASSF1A modulates inflammation and injury in the reperfused murine myocardium.
Jamie Francisco,Jaemin Byun,Yu Zhang,Olivia Berman Kalloo,Wataru Mizushima,Shinichi Oka,Peiyong Zhai,Junichi Sadoshima,Dominic P. Del Re +8 more
TL;DR: It is suggested that myeloid RASSF1A antagonizes I/R-induced myocardial inflammation and may be a promising target in immunomodulatory therapy for the management of acute heart injury.
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