ArticleJournal of the American Heart Association2025
IDO-1 Promotes Pulmonary Vascular Remodeling Via Kynurenine Pathway in Pulmonary Arterial Hypertension.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Cardiometabolic reprogramming in pulmonary arterial hypertension: Implications for right ventricular dysfunction and therapeutic strategies.Chinese herbal medicines · 2026Review
- Divergent Inflammatory and Bioenergetic Metabolomic Signatures Distinguish Methamphetamine-Associated From Idiopathic Pulmonary Arterial Hypertension.Pulmonary circulation · 2026Article
- Advances in the pathogenesis and clinical management of pulmonary hypertension.Medical review (2021) · 2026Review
- Tryptophan metabolism: a potential link between the gut microbiota and pulmonary vascular remodeling in pulmonary hypertension.Frontiers in cellular and infection microbiology · 2026Review
- Circadian clock-gut microbiota axis in pulmonary hypertension: linking gut-lung crosstalk, immune timing and vascular remodeling.Frontiers in physiology · 2026Review
- The gut microbiota-aromatic amino acid axis in cardiovascular disease: pathophysiological roles, translational biomarkers, and therapeutic targeting.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
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Abstract
backgroundActivation of the plasma kynurenine pathway (KP) may contribute to the progression of pulmonary arterial hypertension (PAH). We investigated the functional role and molecular mechanisms of KP activation in PAH.
methodsKP activity was measured in the lungs and plasma of humans and rodents with pulmonary hypertension (PH). KP activity was modulated in lung microvascular endothelial cells in vitro, and through daily oral administration of epacadostat, an inhibitor of IDO-1 (indoleamine 2,3-dioxygenase), the rate-limiting enzyme of the KP, in rats with monocrotaline-induced PH.
resultsIDO-1 expression was increased in peripheral blood mononuclear cells but not in lung tissue of patients with PAH and in rats with monocrotaline-induced PH. Epacadostat prevented KP activation and the development of monocrotaline-induced PH, significantly reduced right ventricular systolic pressure (58±9 versus 42±4 and 46±6 mm Hg for placebo versus epacadostat 50 and 100 mg/kg, respectively,
conclusionsIncreased IDO-1 expression in peripheral blood mononuclear cells may drive KP activation and promote pulmonary vascular remodeling in PAH. Epacadostat prevents the development of monocrotaline-induced PH. These findings suggest a novel approach for the treatment of PAH.
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