PI-PLC signal pathway: a possible pathogenesis link post-myocardial infarction to depression

Depressive disorder in the post-myocardial infarction (MI) period has been associated with increased cardiac morbidity and mortality. The most prominent findings are the increased mortality in patients with depression after myocardial infarction. Despite the extensive studies, the possible pathophysiologic mechanisms behind this association have not been clear. More recently, the data have suggested that both depression and post-MI have been associated with an increased activation status of the platelet. And increased sensitivity to platelet activation has been postulated as one of the mechanisms that may underlie increased vulnerability of depressed post-MI patients to cardiac events, suggesting a pathophysiologic cross-talk between the heart and the brain. Considering the similar changes in serotonin(5-HT) and platelet activation through phosphoinositide (PI)-phospholipase C(PLC) pathway, we guess that PI-PLC signal transduction pathway is a common pathogenesis between depression and post-MI, which mediated by 5-HT resulting in the platelet activation. The article introduces the hypothesis that proposes one possibility. This common mechanism of signal pathway may develop other current theories which are beneficial to future therapies to reduce post-MI depression.