Publications by authors named "Hee-Jung J Kim"
Vascular inflammation regulates endothelial pathophenotypes, particularly in pulmonary arterial hypertension (PAH). Dysregulated lysosomal activity and cholesterol metabolism activate pathogenic inflammation, but their relevance to PAH is unclear. Nuclear receptor coactivator 7 () deficiency in endothelium produced an oxysterol and bile acid signature through lysosomal dysregulation, promoting endothelial pathophenotypes.
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- Vascular inflammation plays a key role in regulating the behavior of endothelial cells, which is especially significant in pulmonary arterial hypertension (PAH), showing complex connections to lysosomal activity and cholesterol metabolism.
- Research identified that the nuclear receptor coactivator 7 (NCOA7) helps maintain lysosomal function and limits inflammation in endothelial cells; when NCOA7 is deficient, it leads to inflammation and worsened PAH symptoms.
- A genetic variant in NCOA7 was linked to PAH severity and mortality, while a computationally designed drug that activates NCOA7 showed potential in reversing PAH symptoms in mice, highlighting a new therapeutic approach.
Background: Left heart disease is the most common cause of pulmonary hypertension (PH) and is frequently accompanied by increases in pulmonary vascular resistance. However, the distinction between phenotypes of PH due to left heart disease with a normal or elevated pulmonary vascular resistance-isolated postcapillary PH (IpcPH) and combined pre- and postcapillary PH (CpcPH), respectively-has been incompletely defined using unbiased methods.
Methods And Results: Patients with extremes of IpcPH versus CpcPH were identified from a single-center record of those who underwent right heart catheterization.