ArticleJournal of the American Heart Association2019
New Molecular Mechanism Underlying Myc-Mediated Cytochrome P450 2E1 Upregulation in Apoptosis and Energy Metabolism in the Myocardium.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Cytochrome P450 2E1 aggravates DXR-induced myocardial injury through imbalanced mitochondrial OPA1.Cell communication and signaling : CCS · 2025Article
- Brain Cytochrome P450: Navigating Neurological Health and Metabolic Regulation.Journal of xenobiotics · 2025Review
- Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review.International journal of molecular sciences · 2024Article
- 11-Hydroxyeicosatetraenoics induces cellular hypertrophy in an enantioselective manner.Frontiers in pharmacology · 2024Article
- Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway.Disease models & mechanisms · 2023Article
- Diallyl sulfide protects against dilated cardiomyopathy via inhibition of oxidative stress and apoptosis in mice.Molecular medicine reports · 2021Article
- Novel rat model of multiple mitochondrial dysfunction syndromes (MMDS) complicated with cardiomyopathy.Animal models and experimental medicine · 2021Article
- SARS-CoV-2 infection aggravates chronic comorbidities of cardiovascular diseases and diabetes in mice.Animal models and experimental medicine · 2021Article
- Microbiota Modulates Cardiac Transcriptional Responses to Intermittent Hypoxia and Hypercapnia.Frontiers in physiology · 2021Article
- Myocardial tissue-specific Dnmt1 knockout in rats protects against pathological injury induced by Adriamycin.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Cellular Effects of Butyrate on Vascular Smooth Muscle Cells are Mediated through Disparate Actions on Dual Targets, Histone Deacetylase (HDAC) Activity and PI3K/Akt Signaling Network.International journal of molecular sciences · 2019Article
- New Molecular Mechanism Underlying Myc-Mediated Cytochrome P450 2E1 Upregulation in Apoptosis and Energy Metabolism in the Myocardium.Journal of the American Heart Association · 2019Article
- Research on the Characteristics of Infrared Radiation Spectra at Zigong Acupoint within Menstrual Cycle of Healthy Female.Evidence-based complementary and alternative medicine : eCAM · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Canonical studies indicate that cytochrome P450 2E1 ( CYP 2E1) plays a critical role in the metabolism of xenobiotics and ultimately participates in tissue damage. CYP 2E1 upregulates in the pathophysiological development of multiple diseases; however, the mechanism of CYP 2E1 upregulation, particularly in heart disease, remains elusive. Methods and Results We found that the level of CYP 2E1 increased in heart tissues from patients with hypertrophic cardiomyopathy; multiple mouse models of heart diseases, including dilated cardiomyopathy, hypertrophic cardiomyopathy, and myocardial ischemia; and HL -1 myocytes under stress. We determined that Myc bound to the CYP 2E1 promoter and activated its transcription by bioinformatics analysis, luciferase activity, and chromatin immunoprecipitation, and Myc expression was modulated by extracellular signal-regulated kinases 1/2 and phosphatidylinositol 3 kinase/protein kinase B pathways under stress or injury in myocardium by signal transduction analysis. In addition, the level of oxidative stress and apoptosis gradually worsened with age in transgenic mice overexpressing CYP 2E1, which was significantly inhibited with CYP 2E1 knockdown. Conclusions Our results demonstrated that CYP 2E1 is likely a sensor of diverse pathophysiological factors and states in the myocardium. Upregulated CYP 2E1 has multiple pathophysiological roles in the heart, including increased oxidative stress and apoptosis as well as energy supply to meet the energy demand of the heart in certain disease states. Our discovery thus provides a basis for a therapeutic strategy for heart diseases targeting Myc and CYP 2E1.
Indexed as
Identifiers
What OpenQuestion holds
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.