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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Immunity, Inflammation, and Oxidative Stress in Heart Failure: Emerging Molecular Targets
TL;DR: It is anticipated that a better understanding of the pathophysiology of HF will open the door for new therapeutic targets, and a one-size-fits-all approach may not be appropriate for all patients with HF, and further clinical trials utilizing molecular targeting in HF may result in improved outcomes.
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Signaling pathways and targeted therapy for myocardial infarction
Qinglu Zhang,Lu Wang,Shi-wen Wang,Hongxin Cheng,Lin Xu,Gaiqin Pei,Yang Wang,Chenying Fu,Yangfu Jiang,ChengQi He,Quan Wei +10 more
TL;DR: In this article , the authors summarize the therapeutic strategies for myocardial infarction (MI) by regulating these associated pathways, which contribute to inhibiting cardiomyocytes death, attenuating inflammation, enhancing angiogenesis, etc.
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Tissue Engineering Strategies for Myocardial Regeneration: Acellular Versus Cellular Scaffolds?
Maribella Domenech,Lilliana Polo-Corrales,Lilliana Polo-Corrales,Jaime E. Ramirez-Vick,Jaime E. Ramirez-Vick,Donald O. Freytes +5 more
TL;DR: The cellular events that take place after an MI are described and how biomaterials have been used to engineer suitable myocardium replacement constructs and how new advanced culture systems will be required to achieve clinical success are described.
Journal ArticleDOI
Unveiling the Role of Inflammation and Oxidative Stress on Age-Related Cardiovascular Diseases.
Arthur José Pontes Oliveira de Almeida,Mathania Silva de Almeida Rezende,Sabine Helena Dantas,Sonaly de Lima Silva,Júlio César Pinheiro Lúcio de Oliveira,Fátima de Lourdes Assunção Araújo de Azevedo,Rayanne Maira Felix Ribeiro Alves,Geovânia Maria Sales de Menezes,Pablo Ferreira dos Santos,Tays Amanda Felisberto Gonçalves,Valérie B. Schini-Kerth,Isac Almeida de Medeiros +11 more
TL;DR: The basics of inflammation and oxidative stress, including the crosstalk between them, are shown, and the implications on age-related CVDs are shown.
Journal ArticleDOI
Assigning matrix metalloproteinase roles in ischaemic cardiac remodelling.
TL;DR: How the understanding of MMPs has evolved from a one-dimensional early focus on measuring MMP activity, monitoring MMP:inhibitor ratios, and evaluating one MMP–substrate pair to the current use of systems biology approaches to integrate the whole MMP repertoire of roles in the left ventricular response to MI is focused on.
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