Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
Should not yet change post-injury management; leaves open whether cytokine targeting improves remodeling in trials.
Fibrosis induced by prolonged inflammation is a major pathophysiological feature of adverse left ventricular remodeling after myocardial infarction and pathological cardiac hypertrophy. Recent reports strongly suggest that the interaction between leukocytes, non-myocytes (mainly cardiac fibroblasts) and cardiomyocytes, possibly mediated by cytokine signaling, plays an important role in controlling the inflammatory reaction after cardiac injury. Therefore, controlling cytokine secretion from resident cardiomyocytes is one plausible strategy for preventing tissue damage.
No takes yet. Share an insight, caveat, or question.
Aoyagi et al. (2012) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: