INNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISITED
By Douglas L. Mann. Circulation Research, 2015
617 citations recorded by the source corpus.
Elevated levels of inflammatory mediators have been identified in patients with heart failure, including heart failure with reduced and preserved ejection fraction, as well as acute decompensated heart failure. Moreover, experimental studies have shown repeatedly that activation of inflammation in the heart provokes left ventricular (LV) remodeling and LV dysfunction. Nonetheless, phase III clinical trials that have attempted to antagonize inflammatory mediators have been negative with respect to the primary end points of the trials, and in some patients, resulted in worsening heart failure and/or death. The following review will discuss how recent developments in the field of innate immunity have advanced our understanding of the role of inflammation in the pathogenesis of heart failure and will discuss the negative outcomes of the existing clinical trials in light of this new information.
Subfields: Cardiology and Cardiovascular Medicine
View Paper: https://www.semanticscholar.org/paper/187d7fd46a097ac4abb19717214fa6cb8b9bbdc9
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In Cardiology and Cardiovascular Medicine
Citations in the corpus
- The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “in more robust inflammatory responses and leukocyte recruitment that induce tissue injury.(13,79,80,83) In this regard, in vivo chimeric mouse models(64) and ex vivo isolated perfused heart studies (in which circulating leukocytes are eliminated)(84)”
- Mitochondrial dysfunction in pathophysiology of heart failure (2018, background): “Mitochondrial dysfunction and inflammation in heart failure Heart failure is associated with heightened inflammatory response, but clinical trials targeting the proinflammatory cytokines have yielded disappointing outcomes (139, 140).”