ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Reduced carboxylesterase 1 is associated with endothelial injury in methamphetamine-induced pulmonary arterial hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Randomized evaluation of the loss-of-function carboxylesterase 1 (CES1) G143E variant on clopidogrel and ticagrelor pharmacodynamics.Clinical and translational science · 2024Trial
- Comparison of Functional and Hemodynamic Parameters Between Methamphetamine-Associated and Idiopathic Pulmonary Arterial Hypertension: Systematic Review and Meta-Analysis.Healthcare (Basel, Switzerland) · 2026Review
- Exposure Pattern Determines Methamphetamine-Induced Right Ventricular Dysfunction and Vascular Remodeling.Comprehensive Physiology · 2026Article
- Methamphetamine-Associated Pulmonary Arterial Hypertension: Impact, Mechanisms, and a Framework for Management.Pulmonary circulation · 2026Review
- Characteristics of the Fatty Acid Composition in Elderly Patients with Occupational Pathology from Organophosphate Exposure.Diagnostics (Basel, Switzerland) · 2025Article
- Treatment Response and Survival in Methamphetamine-Associated Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2025Article
- Drugs and toxins associated with pulmonary arterial hypertension: from established culprits to novel threats.ERJ open research · 2025Review
- Echocardiographic hemodynamics correlate with differences in DOAC-specific bleeding and stroke rates in non-valvular atrial fibrillation.BMC cardiovascular disorders · 2025Article
- Methamphetamine-Associated Pulmonary Arterial Hypertension Is Associated With Worse Right Ventricular Function Than Idiopathic Pulmonary Arterial Hypertension: A Matched Study.Echocardiography (Mount Kisco, N.Y.) · 2025Article
- Review
- Nupr1-mediated vascular smooth muscle cell phenotype transformation involved in methamphetamine induces pulmonary hypertension.Cell biology and toxicology · 2024Article
- Sex-dependent right ventricular hypertrophic gene changes after methamphetamine treatment in mice.European journal of pharmacology · 2021Article
- Regional Variation in Methamphetamine-associated Pulmonary Arterial Hypertension: Who'd Better Call Saul?Annals of the American Thoracic Society · 2021Article
- Toxic Effects of Methamphetamine on Perivascular Health: Co-morbid Effects of Stress and Alcohol Use Disorders.Current neuropharmacology · 2021Review
- RUNX3-dependent oxidative epithelial-to-mesenchymal transition in methamphetamine-induced chronic lung injury.Cell stress & chaperones · 2020Article
- Resveratrol protects the integrity of alveolar epithelial barrier via SIRT1/PTEN/p-Akt pathway in methamphetamine-induced chronic lung injury.Cell proliferation · 2020Article
- TBHQ-Overview of Multiple Mechanisms against Oxidative Stress for Attenuating Methamphetamine-Induced Neurotoxicity.Oxidative medicine and cellular longevity · 2020Review
- Endosomes and Autophagy: Regulators of Pulmonary Endothelial Cell Homeostasis in Health and Disease.Antioxidants & redox signaling · 2019Review
- Methamphetamine Use and Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Methamphetamine and the risk of pulmonary arterial hypertension.Current opinion in pulmonary medicine · 2018Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Pulmonary arterial hypertension is a complication of methamphetamine use (METH-PAH), but the pathogenic mechanisms are unknown. Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH. Although no difference in CYP2D6 expression was seen by lung immunofluorescence, CES1 expression was significantly reduced in endothelium of METH-PAH microvessels. Mass spectrometry analysis showed that healthy pulmonary microvascular endothelial cells (PMVECs) have the capacity to both internalize and metabolize METH. Furthermore, whole exome sequencing data from 18 METH-PAH patients revealed that 94.4% of METH-PAH patients were heterozygous carriers of a single nucleotide variant (SNV; rs115629050) predicted to reduce CES1 activity. PMVECs transfected with this CES1 variant demonstrated significantly higher rates of METH-induced apoptosis. METH exposure results in increased formation of reactive oxygen species (ROS) and a compensatory autophagy response. Compared with healthy cells, CES1-deficient PMVECs lack a robust autophagy response despite higher ROS, which correlates with increased apoptosis. We propose that reduced CES1 expression/activity could promote development of METH-PAH by increasing PMVEC apoptosis and small vessel loss.
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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.