Spatiotemporal Dynamics of Immune Cells in Early Left Ventricular Remodeling After Acute Myocardial Infarction in Mice

Abstract

Myocardial infarction remains a leading cause of morbidity and death. Insufficient delivery of oxygen to the myocardium sets into play a complicated process of repair that involves the temporal recruitment of different immune cells so as to remove debris and necrotic cells expeditiously and to form effective scar tissue. Clearly defined and overlapping phases have been identified in the process, which transitions from an overall proinflammatory to anti-inflammatory phenotype with time. Variations in the strength of the phases as well as in the co-ordination among them have profound consequences. Too strong of an inflammatory phase can result in left ventricular wall thinning and eventual rupture, whereas too strong of an anti-inflammatory phase can lead to cardiac stiffening, arrhythmias, or ventricular aneurisms. In both cases, heart failure is an intermediate consequence with death being the likely outcome. Here, we summarize the role of key immune cells in the repair process of the heart after left ventricular myocardial infarction, along with the associated cytokines and chemokines. A better understanding of the immune response ought to lead hopefully to improved therapies that exploit the natural repair process for mending the infarcted heart.

Sexual dimorphism in acute myocardial infarction-induced acute kidney injury: cardiorenal deteriorating effects of ovariectomy in premenopausal female mice

“…Hemodynamic analysis showed a marked decrease in EF, indicating cardiac dysfunction and enhanced adverse LV remodeling, 7 days post-MI occurring equally in both sexes. The absence of systemic inflammation as observed with undetectable plasma TNF-α levels in mice of both genders, not only correlates with previous studies [ 36 , 37 ] but also rules out any potential correlation between kidney damage and persistent systemic inflammation at 7 days post-MI. With the absence of any pronounced or evident differences between male and premenopausal female mice in systemic hemodynamics and inflammation at 7 days post-MI, the observed sexual dimorphism in MI-induced kidney damage was tracked down to kidney molecular, metabolic, structural, and functional levels.…”

Sex differences in cardiac remodeling post myocardial infarction with acute cigarette smoking

“…In accordance with these observations, we documented a significant increase in the mRNA expression of two major pro-inflammatory markers, IL-6 and TNF-α, at day 7 post-MI in MICS male group only. Both IL-6 and TNF-α spike with initial acute inflammation post-MI (day 1-day 3) and decrease to normal levels during transition to granulation phase post-MI (day 4-day 7) [78]. Persistent inflammation could be the attributing factor to the pronounced cardiac deterioration observed in CS-exposed MI male group that was not seen in the female counterparts.…”

Identification of Immuno-Inflammation-Related Biomarkers for Acute Myocardial Infarction Based on Bioinformatics

“…Immune cells such as neutrophils and monocytes are prominent participants in inflammation during post-infarction repair. 34,35 Dead cardiomyocytes release danger-associated molecular patterns (DAMPs), which bind to pattern recognition receptors of immune cells. Moreover, myocytes surrounding the infarct core secret DAMPs and proinflammatory cytokines and initiate recruitment of circulating immune cells.…”