ArticleMolecular and cellular biochemistry2016
Arginase inhibitor attenuates pulmonary artery hypertension induced by hypoxia.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Changes in Macrophages in Pulmonary Hypertension: A Focus on High-altitude Pulmonary Hypertension.Anatolian journal of cardiology · 2025Review
- Bioactive compound combinations fromFrontiers in pharmacology · 2025Article
- Disruption of DLL4/NOTCH1 Causes Dysregulated PPARγ/AKT Signaling in Pulmonary Arterial Hypertension.bioRxiv : the preprint server for biology · 2024Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Arginine Therapy for Lung Diseases.Frontiers in pharmacology · 2021Review
- Arginase as a Potential Biomarker of Disease Progression: A Molecular Imaging Perspective.International journal of molecular sciences · 2020Review
- Vascular Metabolic Mechanisms of Pulmonary Hypertension.Current medical science · 2020Review
- HIF Oxygen Sensing Pathways in Lung Biology.Biomedicines · 2018Review
- Arginase: A Multifaceted Enzyme Important in Health and Disease.Physiological reviews · 2018Review
- Plasmatic Concentrations of ADMA and Homocystein in Llama (Frontiers in physiology · 2018Article
- Arginase Inhibition Reverses Monocrotaline-Induced Pulmonary Hypertension.International journal of molecular sciences · 2017Article
- Pharmacokinetics and Pharmacodynamics of Promising Arginase Inhibitors.European journal of drug metabolism and pharmacokinetics · 2017Review
- HIF2α-arginase axis is essential for the development of pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- L-citrulline increases arginase II protein levels and arginase activity in hypoxic piglet pulmonary artery endothelial cells.Pulmonary circulationArticle
Corrections and comments
- Retracted
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia-induced pulmonary arterial hypertension (HPAH) is a refractory disease characterized by increased proliferation of pulmonary vascular smooth cells and progressive pulmonary vascular remodeling. The level of nitric oxide (NO), a potential therapeutic vasodilator, is low in PAH patients. L-arginine can be converted to either beneficial NO by nitric oxide synthases or to harmful urea by arginase. In the present study, we aimed to investigate whether an arginase inhibitor, S-(2-boronoethyl)-L-cysteine ameliorates HPAH in vivo and vitro. In a HPAH mouse model, we assessed right ventricle systolic pressure (RVSP) by an invasive method, and found that RSVP was elevated under hypoxia, but was attenuated upon arginase inhibition. Human pulmonary artery smooth muscle cells (HPASMCs) were cultured under hypoxic conditions, and their proliferative capacity was determined by cell counting and flow cytometry. The levels of cyclin D1, p27, p-Akt, and p-ERK were detected by RT-PCR or Western blot analysis. Compared to hypoxia group, arginase inhibitor inhibited HPASMCs proliferation and reduced the levels of cyclin D1, p-Akt, p-ERK, while increasing p27 level. Moreover, in mouse models, compared to control group, hypoxia increased cyclin D1 expression but reduced p27 expression, while arginase inhibitor reversed the effects of hypoxia. Taken together, these results suggest that arginase plays an important role in increased proliferation of HPASMCs induced by hypoxia and it is a potential therapeutic target for the treatment of pulmonary hypertensive disorders.
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