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As an example, immunopathologic vasculopathy in a hypoxic model of pulmonary hypertension was found to be driven by G6PD-induced pro-inflammatory epigenetic signaling — including upregulated expression of pro-inflammatory factors (e.g., tumor necrosis factor-alpha [TNF-α]), increased numbers of activated macrophages, and activated platelets — and conversely, was able to be mitigated with G6PD deficiency ( G6PD-dependent ROS generation is also important in innate immune sensing by macrophages ( Figure 1B-1 )