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Acute myocardial infarction (MI) remains one of the leading causes of mortality and morbidity in the global communities. A prevailing topic that has attracted increasing attentions over the past few decades is the so-called heart-brain interaction, in particular following a major traumatic event such as MI. Increased prevalence of depression and other mental disorders has been recognized in cardiac patients after MI, coronary catheterization, or cardiothoracic surgeries. In this review, we focus on the potential pathogenic mechanisms and pre-clinical transcriptomic evidence for identifying potential mediators of post-MI depression. We first summarize the conventional mechanistic understanding that leads to the current clinical management of post-MI depression with the use of selective serotonin reuptake inhibitors (SSRIs) and cognitive behavior and exercise therapies. We further envisage a possible role played by certain chemokines, e.g., Chemokine (C-X-C motif) ligand 12 (CXCL12) and Chemokine (C-C motif) ligand 2 (CCL22), in serving as signaling molecules to connect the MI-induced heart damage to the pro-depressive changes in brain during the post-MI period. Future in-depth investigations into this chemokine hypothesis will be instrumental in developing new chemokine-targeted therapies for better management of the cardiac patients suffering from post-MI depression.
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