Nasser B. Alsaleh

TL;DR: This review will provide insight into the potential clinical utility of this therapeutic strategy for AMI by outlining the known cardioprotective effects of EETs and underlying mechanisms demonstrated in preclinical models of AMI and discussing preclinical and clinical areas that require further investigation.

TL;DR: The data suggest that the protective effects of EETs involve regulating the autophagic response, which results in a healthier pool of mitochondria in the starved cardiac cells, thereby representing a novel mechanism of promoting survival of cardiac cells.

TL;DR: The data support the hypothesis and show that AgNP-directed mast cell degranulation involves activation of PI3K, PLCγ and an increase in intracellular calcium levels, and it is found that influx of extracellular calcium is required for the cells to degranulate in response to AgNP exposure and is mediated at least partially via the CRAC channels.

TL;DR: In conclusion, inhibition of sEH and EET-induced cardioprotection is maintained in aged mice, however, the loss of protective effects observed in aged CYP2J2 Tr might be attributed to increased levels of DiHOME, oxidative stress and/or decreased PP2A activity.

TL;DR: Key studies and challenges in understanding cellular mechanisms of ENM-mediated immunomodulation and toxicity are highlighted.