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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The Notch pathway: a novel target for myocardial remodelling therapy?
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TL;DR: Modulation of the Notch pathway could become a tool to limit ventricle remodelling and the associated inexorable deterioration of cardiac performance.
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Targeting NLRP3 (Nucleotide-Binding Domain, Leucine-Rich-Containing Family, Pyrin Domain-Containing-3) Inflammasome in Cardiovascular Disorders.
Zheng Wang,Wei Hu,Chenxi Lu,Zhiqiang Ma,Shuai Jiang,Chunhu Gu,Darío Acuña-Castroviejo,Yang Yang +7 more
TL;DR: To further understand the roles of the NLRP3 inflammasome in the cardiovascular system, a comprehensive overview is provided and the remaining questions are discussed to discuss existing problems and potential directions with this issue.
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An Injectable Conductive Three-Dimensional Elastic Network by Tangled Surgical-Suture Spring for Heart Repair.
Chen Song,Chen Song,Xingying Zhang,Leyu Wang,Feng Wen,Kaige Xu,Weirong Xiong,Chuangkun Li,Bingyun Li,Quan Wang,Malcolm Xing,Xiaozhong Qiu +11 more
TL;DR: An injectable bio-spring is developed to form a tangled conductive 3-D network in vivo for MI repair and enhanced the CMs' maturation in synchronous contraction accompanied with high expressions of cardiac-specific proteins in α-actinin and connexin 43.
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The Role of Leukocytes in Diabetic Cardiomyopathy.
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TL;DR: The present review summarizes the role of leukocytes in the complex interplay between diabetes and heart failure, which is critical to the discovery of new targeted therapies for diabetic cardiomyopathy.
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MicroRNAs as important regulators of the NLRP3 inflammasome.
Parvin Zamani,Reza Kazemi Oskuee,Stephen L. Atkin,Jamshid Gholizadeh Navashenaq,Amirhossein Sahebkar +4 more
TL;DR: The current understanding of the role of miRNAs in the regulation of NLRP3 inflammasome complexes and their impact on the pathogenesis of inflammatory disease processes is summarized.
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