Kumar et al. (195) showed that AFs obtained from humans with PAH and calves with hypoxia-induced PAH secreted exosomes containing complement C3, which mediated BMDM activation toward a proinflammatory and metabolically altered phenotype in vitro, and the latter was characterized by increased aerobic glycolysis and the accumulation of succinic acid. Here, C3 is linked to pulmonary arterial hypertension.