Extracellular Vesicle-Mediated Neuroinflammation in the Heart-Brain Axis Post-Myocardial Infarction: Mechanistic Insights and Cellular Interactions

Recent evidence has led to consider myocardial infarction (MI) not only a mere disease of the heart, but a more complex disease mediating pathological response of many distant organs, including the brain.

MI has a shortand long-term deleterious impact on brain homeostasis and thereby, plays a causative role in occurrence of anxiety, depression, and cognitive deficits in MI patients.

In addition to increased coagulation and thrombosis, factors such as enhanced systemic inflammation and exosomes released from the injured heart may favor brain damage after MI by critically altering glial cell responses in the brain and thereby, promoting chronic neuroinflammation.

Specifically, the astrocyte-microglia dialogue that is needed for proper maintenance of homeostatic conditions in the brain may be altered post-MI.

However, it is unclear if and how MI triggers regional glia cell responses and how they transform to global chronic neuroinflammation with consequences for neuronal health.

By identifying spatiotemporal neuroinflammatory signatures and their molecular basis, the current study will generate first systematic mechanistic knowledge on how cardiac derived triggers initiate and propagate chronic neuroinflammation.

Establishing appropriate methods to isolate, characterize, and track cardiac-derived exosome represents an essential first step prior to future in vivo approaches that may be basis for the development of predictive biomarkers of neuroiflammatory processes post-MI.