This talk will focus on the recently recognized heterogeneity of resident macrophages during development and in the adult heart, which has led to confusion about their roles in cardiac homeostasis, in repsone to injury and whether they represent potential therapeutic targets.

Both acute and chronic regulation of cardiac remodeling requires a balance in the modulation of various myeloid cell populations. Knowing which populations to target, when during the remodeling process to target them and how best to do so therapeutically will be the focus of this talk. Although early to confirm at this time, this talk may touch upon the impact of infiltrating myeloid cells on the heart in the context of COVID-19.

In the past decade, substantial evidence has shown a major role of the immune system in the pathogenesis of diseases such as cancer and hypertension. In most hypertensive individuals, high blood pressure is primary and associated with modifiable risk factors like salt intake. In response to high salt intake, NaCl concentrates in tissues over time and stimulates the formation of different T-cell subsets that can set the stage for hypertension development. High NaCl levels can promote the polarization of T CD4 helper cells into the pro-inflammatory TH17 phenotype in a SGK1-dependent manner. Previous data has shown that memory T cells play a vital role in the pathogenesis of hypertension; long-lived memory cells can generate a systemic inflammatory response through mobilization to organs and release of cytokines, leading to multiple organ damage seen in hypertension.

T cells are important mediators of cardiac inflammation and remodeling, and inhibition of their trafficking through the heart may offer a beneficial therapeutic direction, which will be the focus of this talk. Depending on the speaker's ability to do so, the talk could be related to the cytokine storm that precipitates worsened outcomes in COVID-19 patients.

This talk will focus primarily on the ability to pharmacologically manipulate leukocytes to lessen their inflammatory effects and promote would repair following cardiac injury or during heart failure.

Acute systemic inflammatory syndromes, such as endotoxemia, elicit detrimental multi-organ responses. The heart is particularly susceptible to an acute inflammatory response resulting in myocardial dysfunction which often leads to death. A stress-induced metabolism of N-3 and N-6 polyunsaturated fatty acids (PUFAs) will generate numerous bioactive lipid mediators with beneficial or adverse effects. Cytochrome P450 (CYP) derived epoxylipid mediators may be further hydrolyzed to diol metabolites by soluble epoxide hydrolase (sEH). Emerging evidence suggests epoxylipids can exert cardioprotective effects by modulating the NLRP3 inflammasome pathway. This study investigated whether cardiomyocyte specific sEH knockdown can preserve cardiac function and attenuate inflammation in a model of acute lipopolysaccharide (LPS) injury.