Published online Oct 26, 2018. doi: 10.4330/wjc.v10.i10.123
Peer-review started: May 29, 2018
First decision: June 14, 2018
Revised: June 20, 2018
Accepted: June 28, 2018
Article in press: June 28, 2018
Published online: October 26, 2018
Immune system activation and dysfunction characterize the early phase of reperfusion after a myocardial infarction (MI). Despite initially neglected, adaptive immunity has been recently showed to play an important role in this setting. In fact, the immune system can recognize sequestered antigens released by the necrotic tissue, initiating a deleterious autoimmune vicious circle leading to worse outcome. In their recent work, Angelini et al shed the light on a new feature of post-MI which involves two “old players” of post-ischemic myocardial injury: CD31 and matrix metalloproteinase (MMP)-9. Specifically, the authors showed that an enhancement of MMP-9 release could determine the cleavage of inhibitory CD31 from CD4+ T-cells surface in patients with Acute Coronary Syndromes (ACS). These findings open the room for new studies investigating the role of MMP9 in other pathological processes associated with a reduction of CD31 functionality, such as plaque instability and rupture. Of interest, in the case of a causative role for CD31 shedding in ACS would be confirmed, there might be a potential role for the administration of CD31 protein or analogue compounds to blunt post-ischemic cardiac inflammation and improve ACS outcome.
Core tip: CD31 and matrix metalloproteinases (MMP)-9 are known mediators that are upregulated during reperfusion after cardiac ischemia. By inhibiting T-cell receptor-dependent lymphocyte activation, the functional CD31 could reduce post-ischemic inflammatory response; while MMP-9 is deeply involved in inflammatory cell recruitment and myocardial remodeling. A recent paper published in European Heart Journal linked these mediators by showing CD31 cleavage to be MMP-9 dependent in patients with acute coronary syndromes (ACS). Whether this process is causative of ACS or rather its effect still needs to be clarified.