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In this issue of Circulation Research , Marsboom et al1 describe a novel involvement of a mitochondrial fission regulatory pathway that is likely to be of great importance in pulmonary arterial hypertension (PAH)-associated smooth muscle remodeling. Data in the study provide evidence that this process appears to be controlled by activation of hypoxia inducible factor-1α (HIF-1α). As illustrated in the model in Figure, the stabilization or activation of HIF-1α in PAH is shown to promote mitochondrial fission by cyclin B1/CDK1-dependent phosphorylation of dynamin-related protein-1 (DRP1) at serine-616. The CDK1-cyclin B-dependent regulation of tubular mitochondria fragmentation by DRP1 was identified in previous studies as a regulator of the even distribution of mitochondria during mitosis in HeLa cells.2 Data in the study of Marsboom et al1 document how this process appears to be essential for the in vitro proliferation of pulmonary arterial smooth muscle cells from human hypertensive patients. In addition, evidence is provided for these mechanisms appearing to be a prominent contributing factor to pulmonary arterial remodeling in several different models of PAH.Figure. Model showing how conditions associated with pulmonary hypertension development promote hypoxia inducible factor (HIF)-1α regulation of pulmonary arterial smooth proliferative remodeling that appears to be controlled by a cyclin B1/CDK1-mediated phosphorylation of dynamin-related protein-1 (DRP1), which causes mitochondrial fission needed for their even distribution of during mitosis. The model also highlights approaches described in the text that were used to elucidate mechanisms.Article, see p 1484As described in the article of Marsboom et al,1 PAH is disorder in which small pulmonary arteries are obstructed, constricted, and inflamed in a manner that increases pulmonary vascular resistance, and this promotes right ventricular hypertrophy and eventually failure. Previous work …

circulation research

Novel Role for the Regulation of Mitochondrial Fission by Hypoxia Inducible Factor-1α in the Control of Smooth Muscle Remodeling and Progression of Pulmonary Hypertension