ArticleAmerican journal of respiratory and critical care medicine2013
Endothelial indoleamine 2,3-dioxygenase protects against development of pulmonary hypertension.
Article in American journal of respiratory and critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- The tryptophan-kynurenine pathway in cardiovascular diseases: mechanistic insights and therapeutic opportunities.Frontiers in cardiovascular medicine · 2026Review
- IDO-1 Promotes Pulmonary Vascular Remodeling Via Kynurenine Pathway in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2025Article
- Breathing New Life into Pulmonary Arterial Hypertension Treatment: Targeting Serotonin Synthesis with an Inhalation Approach.American journal of respiratory cell and molecular biology · 2025Article
- Physiologic relevance of the transpulmonary metabolome in connective tissue disease-associated pulmonary vascular disease.JCI insight · 2025Article
- Kynurenine Pathway in Respiratory Diseases.International journal of tryptophan research : IJTR · 2024Review
- The role of the kynurenine pathway in cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- A Review of the Evidence for Tryptophan and the Kynurenine Pathway as a Regulator of Stem Cell Niches in Health and Disease.International journal of tryptophan research : IJTR · 2024Review
- COVID-19. Biology, pathophysiology, and immunology: a pathologist view.Pathologica · 2023Review
- Clinical, radiological and pathological findings in patients with persistent lung disease following SARS-CoV-2 infection.The European respiratory journal · 2022Article
- Indoleamine 2,3-Dioxygenase 1 Deletion-Mediated Kynurenine Insufficiency in Vascular Smooth Muscle Cells Exacerbates Arterial Calcification.Circulation · 2022Article
- Unbalanced IDO1/IDO2 Endothelial Expression and Skewed Keynurenine Pathway in the Pathogenesis of COVID-19 and Post-COVID-19 Pneumonia.Biomedicines · 2022Review
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- Endothelial cells in the pathogenesis of pulmonary arterial hypertension.The European respiratory journal · 2021Review
- The pathogenic role of epithelial and endothelial cells in early-phase COVID-19 pneumonia: victims and partners in crime.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Review
- Article
- Carbonic anhydrase inhibition improves pulmonary artery reactivity and nitric oxide-mediated relaxation in sugen-hypoxia model of pulmonary hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Emerging Roles on Immunological Effect of Indoleamine 2,3-Dioxygenase in Liver Injuries.Frontiers in medicine · 2021Review
- Covid-19 Interstitial Pneumonia: Histological and Immunohistochemical Features on Cryobiopsies.Respiration; international review of thoracic diseases · 2021Article
- Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism.International journal of molecular sciences · 2020Review
- Carbonic Anhydrase Inhibition Ameliorates Inflammation and Experimental Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleA proliferative and apoptosis-resistant phenotype in pulmonary arterial smooth muscle cells (PASMCs) is key to pathologic vascular remodeling in pulmonary hypertension (PH). Expression of indoleamine-2,3-dioxygenase (IDO) by vascular endothelium is a newly identified vasomotor-regulatory mechanism also involved in molecular signaling cascades governing vascular smooth muscle cell (vSMC) plasticity.
objectivesTo investigate the therapeutic potential of enhanced endothelial IDO in development of PH and its associated vascular remodeling.
methodsWe used loss and gain of function in vivo studies to establish the role and determine the therapeutic effect of endothelial IDO in hypoxia-induced PH in mice and monocrotaline-induced PH in rats. We also studied PASMC phenotype in an IDO-high in vivo and in vitro tissue microenvironment. MEASUREMENTS AND MAIN
resultsThe endothelium was the primary site for endogenous IDO production within mouse lung, and the mice lacking this gene had exaggerated hypoxia-induced PH. Conversely, augmented pulmonary endothelial IDO expression, through a human IDO-encoding Sleeping Beauty (SB)-based nonviral gene-integrating approach, halted and attenuated the development of PH, right ventricular hypertrophy, and vascular remodeling in both preclinical models of PH. IDO derived from endothelial cells promoted apoptosis in PH-PASMCs through depolarization of mitochondrial transmembrane potential and down-regulated PH-PASMC proliferative/synthetic capacity through enhanced binding of myocardin to CArG box DNA sequences present within the promoters of vSMC differentiation-specific genes.
conclusionsEnhanced endothelial IDO ameliorates PH and its associated vascular structural remodeling through paracrine phenotypic modulation of PH-PASMCs toward a proapoptotic and less proliferative/synthetic state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.