The inflammatory response in myocardial injury, repair and remodeling
By Nikolaos G. Frangogiannis. Nature Reviews Cardiology, 2014
1,567 citations recorded by the source corpus.
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.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/20e5abdff0c6739a973a9b4a8af58eeb50c9b97c
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Citations in the corpus
- The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “tory response may be involved in the pathogenesis of adverse remodeling and HF after MI.(191)”
- Pathophysiology of Myocardial Infarction (2015, neutral): “of patients with distinct pathophysiologic characteristics to implement personalized treatment strategies (111, 113).”