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This process yields an excess of reactive oxygen species (ROS), which impairs endothelial function, reduces the bioavailability of nitric oxide (NO), and triggers the release of tissue factor (TF), cumulatively contributing to the formation of microclots in the pulmonary vasculature [3,4]

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Upon binding, CD226 acts through VAV1 to induce ERK signaling critical in augmenting TCR activation and perhaps natural killer cell activation (7, 92, 93)