New insights into the pathology of pulmonary hypertension: implication of the miR‐210/ISCU1/2/Fe‐S axis

• Published in: EMBO molecular medicine Vol. 7; no. 6; pp. 689 - 691
• Main Authors: Tang, Haiyang, Ayon, Ramon J, Yuan, Jason X‐J
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01-06-2015; BlackWell Publishing Ltd; Springer Nature
• Subjects: Animals; Closeup; EMBO21; EMBO35; Female; Genetic Predisposition to Disease; Humans; Hypertension, Pulmonary - genetics; Hypoxia - complications; Iron - deficiency; Iron-Sulfur Proteins - genetics; MicroRNAs - genetics; Sulfur - deficiency
• ISSN: 1757-4676; 1757-4684
• DOI: 10.15252/emmm.201505160

Elevated pulmonary arterial pressure in patients with pulmonary hypertension (PH) is mainly caused by increased pulmonary vascular resistance (PVR), due primarily to sustained pulmonary vasoconstriction and excessive pulmonary vascular remodeling. According to the current classification, PH has been classified into five categories based on etiology (Simonneau
et al
,
2013
). Among them, group 1 or pulmonary arterial hypertension (PAH) is a rare but progressive and deadly disease affecting ~1–10 per 1 million people. Despite expanding treatment options to ameliorate patients' symptoms, PAH remains a devastating disease with a poor long‐term prognosis.
Graphical Abstract
Yuan and colleagues discuss on the paper published in this issue showing that hypoxia‐inducible miR‐210 down‐regulates its targets ISCU1/2 to regulate pulmonary vascular and endothelial levels of Fe‐S clusters upon acquired injury or mutations.