CFL1 and pulmonary arterial hypertension: Findings on the source of cytoplasmic [Ca2+], the participation of caldesmon in the regulation of contraction, alterations in RhoA/ROCK sensitivity and the non-involvement of cofilin and LIM kinase (LIMK) in PAH smooth muscle contraction open new avenues to modulation of the excessive contraction taking place in pulmonary arterial hypertension.