Moreover, we have demonstrated that in vivo treatment of mice with δ-aminolevulinic acid (ALA), a heme-synthesis precursor that promotes PpIX-elicited activation of sGC, attenuated hypoxia-induced pulmonary hypertension via preserving sGC/cGMP-dependent vasodilation [16,17]. Here, SGCB is linked to pulmonary arterial hypertension.