A research group led by Professor Kiyoshi Hirahara, Associate Professor Chiaki Iwamura, and Visiting Researcher Sachiko Kuriyama from the Graduate School of Medicine, Chiba University, in collaboration with Juntendo University, has revealed that the protein MYL9/12 (Note 1) plays a role in inducing vascular remodeling (Note 3) and inflammation in the intractable disease pulmonary hypertension (Note 2). This research achievement was published online on July 2, 2026 (US Eastern Time) in Circulation Research, an international medical journal published by the American Heart Association. (Paper here: 10.1161/CIRCRESAHA.125.327791) Figure: Research Achievements and Future Prospects ■ Background of the Research Pulmonary hypertension is an intractable disease in which the walls of the pulmonary arteries thicken and harden, narrowing the blood vessels. Current treatments make it difficult to restore the thickened blood vessels to their original state. It was known that the hypoxic state of blood vessels was deeply involved in the onset of the disease, but the mechanism by which vascular changes and inflammation were caused remained unclear. Furthermore, a "right heart catheterization" procedure, which involves inserting a thin tube from the blood vessels to the heart, is necessary for the definitive diagnosis and assessment of pulmonary hypertension, but it places a significant burden on patients. Therefore, the key challenges were: 1) elucidating the mechanism of disease onset and exploring new therapeutic methods, and 2) developing biomarkers that can complement right heart catheterization and allow for simpler assessment of the disease state or measurement of its severity. ■ Key Research Findings ● Identification of a protein crucial for the worsening of pulmonary hypertension: It was discovered that when blood vessels are in a hypoxic state, the protein MYL9/12 is released from platelets and abnormal pulmonary vascular endothelial cells. The accumulation of MYL9/12 in t