T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells

<div>Schematic presentation of proposed mechanism. Activated T lymphocytes shed exosomes containing ERK1/2 and MEK1/2 kinases. These exosomes taken up by endothelial cells cause upregulation of NOX4 leading to oxidative stress and enhanced proliferation.</div>

Oxidative Medicine and Cellular Longevity

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Figure 9

Figure 9: T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells 

Figure 9 | T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells 