Jason S. Hong

This study shows that impaired BCAA metabolism promotes ferroptosis, leading to pulmonary arterial hypertension and associated liver disease, and that targeting BCAA metabolism can alleviate these effects.

This study shows that loss of ROR2 leads to endothelial dysfunction in PAH through inappropriate integrin beta 1 activation, impairing barrier integrity and angiogenesis.

This study identifies subclinical liver dysfunction clusters in PAH patients and links them to pulmonary vascular resistance and immune signaling changes.

This study identifies EBF1 as a regulator of embryonic artery formation and shows its reactivation in pulmonary arterial hypertension drives pathological vascular remodeling.

This study identifies a 12-gene BTB signature, shows CDH5 as a core component, and demonstrates that BIA disrupts the BTB to enhance chemotherapy delivery and efficacy in GBM.

The paper identifies rare FOXF1 missense variants in PAH patients, shows dysregulated FOXF1 expression in PAH lungs, and identifies downstream targets linked to PAH pathogenesis.

This study shows that targeting Snai1 in the right ventricle rescues pulmonary hypertension-induced failure by reducing EndMT, fibrosis, and FMT through a LOXL2-dependent mechanism.

The paper identifies a gene co-expression module, the pink module, associated with PAH severity, genetic risk, vascular cell types, and therapeutic targets through multiomics integration.

The paper identifies a Tm4sf1-marked endothelial stem/progenitor cell subpopulation in rat lungs associated with PAH and shows its relevance to human PAH through transcriptomic analysis.

This study examines how fructose affects metabolic and transcriptomic responses in genetically diverse mice, identifying strain-specific pathways and regulators involved in metabolic dysfunctions.