ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Supplemental oxygen induced cardiovascular pathophysiology in an end-of-life care model in mice.Physiological reports · 2026Article
- Review
- SHP2 genetic variants in NSML-associated RASopathies disrupt the PZR-IRX transcription factor signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Influence of age and sex on physical, cardiac electrical and functional alterations in progressive hyperoxia treatment: A time course study in a murine model.Experimental gerontology · 2024Article
- Cardioprotective Effects of Dexmedetomidine in an Oxidative-Stress In Vitro Model of Neonatal Rat Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Macrophage-Targeted Nanomedicines for ARDS/ALI: Promise and Potential.Inflammation · 2022Review
- Extracellular matrix and cyclic stretch alter fetal cardiomyocyte proliferation and maturation in a rodent model of heart hypoplasia.Frontiers in cardiovascular medicine · 2022Article
- The implications of hyperoxia, type 1 diabetes and sex on cardiovascular physiology in mice.Scientific reports · 2021Article
- Impact of hyperoxia on cardiac pathophysiology.Journal of cellular physiology · 2019Review
- Cardiovascular Risks Associated with Gender and Aging.Journal of cardiovascular development and disease · 2019Review
- Hyperoxia-induced cardiotoxicity and ventricular remodeling in type-II diabetes mice.Heart and vessels · 2018Article
- Proteomic analysis of mitochondrial proteins in the guinea pig heart following long-term normobaric hyperoxia.Molecular and cellular biochemistry · 2017Article
- Kvβ1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity.American journal of physiology. Heart and circulatory physiology · 2017Article
- Deletion of Kvβ1.1 subunit leads to electrical and haemodynamic changes causing cardiac hypertrophy in female murine hearts.Experimental physiology · 2016Article
- High level of oxygen treatment causes cardiotoxicity with arrhythmias and redox modulation.Toxicology and applied pharmacology · 2015Article
- The effect of disease on human cardiac protein expression profiles in paired samples from right and left ventricles.Clinical proteomics · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Ventricular arrhythmias account for high mortality in cardiopulmonary patients in intensive care units. Cardiovascular alterations and molecular-level changes in response to the commonly used oxygen treatment remains unknown. In the present study we investigated cardiac hypertrophy and cardiac complications in mice subjected to hyperoxia. Results demonstrate that there is a significant increase in average heart weight to tibia length (22%) in mice subjected to hyperoxia treatment vs. normoxia. Functional assessment was performed in mice subjected to hyperoxic treatment, and results demonstrate impaired cardiac function with decreased cardiac output and heart rate. Staining of transverse cardiac sections clearly demonstrates an increase in the cross-sectional area from hyperoxic hearts compared with control hearts. Quantitative real-time RT-PCR and Western blot analysis indicated differential mRNA and protein expression levels between hyperoxia-treated and control left ventricles for ion channels including Kv4.2 (-2 ± 0.08), Kv2.1 (2.54 ± 0.48), and Scn5a (1.4 ± 0.07); chaperone KChIP2 (-1.7 ± 0.06); transcriptional factors such as GATA4 (-1.5 ± 0.05), Irx5 (5.6 ± 1.74), NFκB1 (4.17 ± 0.43); hypertrophy markers including MHC-6 (2.17 ± 0.36) and MHC-7 (4.62 ± 0.76); gap junction protein Gja1 (4.4 ± 0.8); and microRNA processing enzyme Drosha (4.6 ± 0.58). Taken together, the data presented here clearly indicate that hyperoxia induces left ventricular remodeling and hypertrophy and alters the expression of Kv4.2 and MHC6/7 in the heart.
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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.