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Published on: April 14, 2023
Mental disorders after myocardial infarction: potential mediator role for chemokines in heart-brain interaction?
Parth Patel1, Feiyan Yang2, Dumitru A Iacobas3
1Department of Biology, College of Humanities and Sciences, Virginia Commonwealth University, Richmond, VA, USA.
Insights
Myocardial infarction (MI) survivors often experience depression. This review explores how heart damage may trigger brain changes, highlighting chemokines like CXCL12 and CCL22 as potential therapeutic targets for post-MI depression.
Area of Science:
- Cardiology
- Neuroscience
- Psychiatry
Background:
- Acute myocardial infarction (MI) is a major cause of global mortality and morbidity.
- Cardiac patients frequently exhibit increased depression and mental health disorders post-MI, surgery, or catheterization.
- The heart-brain interaction following MI is a growing area of research.
Purpose of the Study:
- To review pathogenic mechanisms of post-MI depression.
- To identify potential mediators of depression after MI using pre-clinical transcriptomic evidence.
- To explore the role of chemokines in connecting cardiac damage to brain changes.
Main Methods:
- Literature review of conventional and novel mechanistic understanding of post-MI depression.
- Analysis of pre-clinical transcriptomic data to identify potential mediators.
- Focus on chemokine signaling pathways, specifically CXCL12 and CCL22.
Main Results:
- Conventional treatments for post-MI depression include SSRIs, cognitive behavioral therapy, and exercise.
- Chemokines such as CXCL12 and CCL22 are proposed as signaling molecules linking MI-induced cardiac damage to pro-depressive brain changes.
- Transcriptomic evidence supports the role of specific mediators in the heart-brain axis.
Conclusions:
- Existing therapies for post-MI depression have limitations.
- Chemokines represent a promising therapeutic target for managing depression in cardiac patients.
- Further research into chemokine-targeted therapies is crucial for improving patient outcomes.
Abstract:
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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