CX3CR1 and pulmonary arterial hypertension: In parallel, the loss of CX3CR1 favored M1 macrophage polarization, and this shift from M2 to M1 abrogated the ability of macrophage-conditioned medium to induce PASMC proliferation in vitro, suggesting a pathophysiological role of CX3CR1 via M2 macrophage polarization in PAH [87].