Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction

Abstract

The brain is susceptible to acute MI and chronic heart failure. Immune activation may interconnect heart and brain dysfunction, a finding that provides a foundation for strategies to improve heart and brain outcomes.

β‐ RA reduces DMQ /CoQ ratio and rescues the encephalopathic phenotype in Coq9 R239X mice

“…While we were not able to reveal how the peripheral tissues communicate with the brain in this situation, a recent study about gene therapy in a mouse model of Leigh syndrome also suggests that the correction of the gene defect in peripheral tissues is important to reduce brain pathology (Di Meo et al , ). The studies about the kidney–brain, heart–brain, or liver–brain cross‐talk, as well as the presence of a gut–brain axis, would support the concept of an influence of peripheral tissues in the brain pathology, and reactive astrogliosis in particular (Mayo et al , ; Butterworth, ; Rothhammer et al , , ; Miranda et al , ; Thackeray et al , ).…”

Ex vivo characterization of neuroinflammatory and neuroreceptor changes during epileptogenesis using candidate positron emission tomography biomarkers

“…22,40 However, in our study TSPO expression does not reflect the astroglial activation as determined by 18 F-deprenyl autoradiography. 42 It is possible that the discrepancies reflect differences between species and neuroinflammation responses in these models. These results contradict previous studies in a mouse model of SE, where late astrogliosis was paralleled by an increase of TSPO tracer uptake, 22 but are consistent with previous findings from rodent models of neuroinflammation in Alzheimer's disease 41 and myocardial infarction.…”

“…These results contradict previous studies in a mouse model of SE, where late astrogliosis was paralleled by an increase of TSPO tracer uptake, 22 but are consistent with previous findings from rodent models of neuroinflammation in Alzheimer's disease 41 and myocardial infarction. 42 It is possible that the discrepancies reflect differences between species and neuroinflammation responses in these models.…”

Imaging the Molecular Footprints of the Heart–Brain Axis in Cardiovascular Disease

“…This TSPO upregulation was not limited to the heart. Diffuse global neuroinflammation was identified in an identical biphasic pattern, with elevated signal at 1 wk, baseline levels at 4 wk, and reelevated signal at 8 wk (11). At both time points, TSPO colocalized to CD68-positive microglia within the cortex, suggesting cognitive consequences.…”

“…To evaluate the influence of cardiac ischemic injury on the brain, we occluded a coronary artery in mice and serially assessed cardiac and neuroinflammation using PET of mitochondrial translocator protein (TSPO) as a marker of activated peripheral macrophages and brain microglia (11). At 1 wk after myocardial infarction, mice exhibited a markedly higher TSPO PET signal emanating from the infarct territory, colocalized to infiltrating CD68-positive macrophages (Fig.…”