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In this issue of the Journal, Peng et al5 report that CH ulmonary hypertension is thought to result from a number of disorders, including left heart disease, lung disease, and chronic thromboembolic disease.1,2 It is characterized by progressive remodeling of the distal pulmonary arteries, such as medial hypertrophy, intimal proliferative and fibrotic changes, adventitial thickening with moderate perivascular inflammatory infiltrates, and thrombotic lesions.1–4 Chronic hypoxia (CH) induces such vascular remodeling not only in the pulmonary artery but also in the pulmonary vein P

circulation journal

Roles of Canonical Transient Receptor Potential 6 in Basal [Ca&lt;sup&gt;2+&lt;/sup&gt;]&lt;sub&gt;i&lt;/sub&gt; Regulation in Pulmonary Venous Smooth Muscle Cells Under Chronic Hypoxia-Induced Hypertension