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Clec4e signalling influences left-ventricular functional recovery in a murine model of myocardial ischemia-reperfusion injury


 
 
 The acute inflammatory response contributes substantially to functional recovery and remodelling of the left ventricle after acute ischemic injury. Previously, we have shown that the C-Type Lectin Receptor CLEC4E plays a role in early leukocyte recruitment during the acute inflammatory response of ischemia-reperfusion injury (I/R). However, the role of CLEC4E signalling in functional recovery of the left ventricle after I/R remains unknown. Therefore, we studied the chronic inflammatory response and left-ventricular remodelling in murine gene deletion model of Clec4e, subjected to I/R.
 
 
 
 In anesthetized C57Bl6/J wild-type (n=14) and Clec4e−/− (n=13) mice, we transiently occluded the left-descending artery for 60 min, followed by 4 weeks reperfusion (I/R). A blood sample was collected at 90 minutes reperfusion to measure high-sensitivity troponin I (TnI) levels, as a surrogate marker of cardiac damage. At 4 weeks, mice underwent MRI (7T) to investigate the effect of Clec4e-gene deletion on LV-remodelling.
 
 
 
 Plasma TnI-levels showed no statistical difference between both groups, indicating that the initial insult was comparable. In wild-type mice, plasma TnI-levels negatively correlated with ejection fraction (EF, R2=0.92 p<0.0001) at 4 weeks I/R, while Clec4e−/− mice showed preserved EF, irrespective of 90 minutes TnI-levels. MRI-analysis at 4 weeks after I/R showed significantly smaller end-diastolic and end-systolic volumes in Clec4e−/− mice, together with a trend towards a higher ejection fraction, suggesting better preserved structural and functional LV-remodelling (Fig.1).
 
 
 
 The inflammatory leukocyte-associated Clec4e signalling pathway impairs functional recovery of the left ventricle after myocardial I/R injury. Inhibition of the Clec4e receptor may be a promising strategy in the treatment of ischemic injury.
 Figure 1
 
 
 
 Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): Scholarship Ir. Jozef en Mevr. Reinhilde De Swerts 2018-2022 by the Royal Academy of Medicine of Belgium
