Does blockade of NKG2D/NKG2D ligand interaction attenuate cardiac remodelling after myocardial infarction?
Blockade of NKG2D/NKG2D ligand interaction attenuates cardiac remodelling after myocardial infarction, suggesting a role for the immunosurveillance system in post-infarct heart failure.
AimsAccumulating evidence demonstrates that cardiomyocyte death contributes to the onset and progression of heart failure (HF) after myocardial injury. Recent studies revealed that immune/inflammatory reactions play important roles in cardiovascular diseases. However, it remains unclear whether immunosurveillance system, which eliminates cytopathic cells, including infected or malignant cancer cells, is involved in cardiomyocyte death, though cardiomyocytes are exposed to pathological stresses during post-infarct remodelling. The aim of this study is to clarify the pathophysiological significance of Natural Killer Group 2 member D (NKG2D)/NKG2D ligand (NKG2DL)-mediated cell death in HF after myocardial infarction (MI).
Matsumoto et al. (Wed,) studied this question.