4.7 Article

Metabolic profile in endothelial cells of chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension

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Summary: This study comprehensively analyzed the endothelial function, molecular signature, and mitochondrial profile of CTEPH-derived endothelial cells, revealing a hyperproliferative phenotype with increased expression of adhesion molecules, decreased apoptosis, eNOS activity, and migration capacity compared to healthy endothelial cells. Furthermore, CTEPH-EC exhibited altered mitochondrial dynamics, increased mitochondrial respiration, and an unbalanced production of reactive oxygen species and antioxidants. Modulation of redox, mitochondrial homeostasis, and adhesion molecule overexpression could be potential novel targets and biomarkers in treating CTEPH.

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