ArticlePhysiological genomics2005
Gene expression and phenotypic characterization of mouse heart after chronic constant or intermittent hypoxia.
Article in Physiological genomics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 84 citations in OpenAlex.
- Roxadustat (FG-4592): Correction of Anemia in Incident Dialysis Patients.Journal of the American Society of Nephrology : JASN · 2016Trial
- Signaling pathway alterations in hearts of a porcine model harboring a β-myosin heavy chain (MYH7-R403Q) gene variant.Journal of molecular and cellular cardiology plus · 2025Article
- Theory and Applications of the (Cardio) Genomic Fabric Approach to Post-Ischemic and Hypoxia-Induced Heart Failure.Journal of personalized medicine · 2022Article
- Article
- Roxadustat as treatment for a blood transfusion-dependent maintenance hemodialysis patient: A case report and review of literature.World journal of clinical cases · 2021Article
- Article
- Microbiota Modulates Cardiac Transcriptional Responses to Intermittent Hypoxia and Hypercapnia.Frontiers in physiology · 2021Article
- MKRN1 Ubiquitylates p21 to Protect against Intermittent Hypoxia-Induced Myocardial Apoptosis.Oxidative medicine and cellular longevity · 2021Article
- Article
- Powerful quantifiers for cancer transcriptomics.World journal of clinical oncology · 2020Review
- Translating Translation to Mechanisms of Cardiac Hypertrophy.Journal of cardiovascular development and disease · 2020Review
- Sexual dimorphism in cardiac transcriptome associated with a troponin C murine model of hypertrophic cardiomyopathy.Physiological reports · 2020Article
- Article
- Expression and Correlation of Hypoxia-Inducible Factor-1α (HIF-1α) with Pulmonary Artery Remodeling and Right Ventricular Hypertrophy in Experimental Pulmonary Embolism.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- The Effects of Experimental Sleep Apnea on Cardiac and Respiratory Functions in 6 and 18 Month Old Dystrophic (mdx) Mice.PloS one · 2016Article
- Intermittent Hypoxia Alters Gene Expression in Peripheral Blood Mononuclear Cells of Healthy Volunteers.PloS one · 2015Article
- Regulation of hypoxia-induced pulmonary hypertension by vascular smooth muscle hypoxia-inducible factor-1α.American journal of respiratory and critical care medicine · 2014Article
- Genetic analysis of hypoxia tolerance and susceptibility in Drosophila and humans.Annual review of genomics and human genetics · 2013Review
- Identification of genes underlying hypoxia tolerance in Drosophila by a P-element screen.G3 (Bethesda, Md.) · 2012Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic constant hypoxia (CCH), such as in pulmonary diseases or high altitude, and chronic intermittent hypoxia (CIH), such as in sleep apnea, can lead to major changes in the heart. Molecular mechanisms underlying these cardiac alterations are not well understood. We hypothesized that changes in gene expression could help to delineate such mechanisms. The current study used a neonatal mouse model in CCH or CIH combined with cDNA microarrays to determine changes in gene expression in the CCH or CIH mouse heart. Both CCH and CIH induced substantial alterations in gene expression. In addition, a robust right ventricular hypertrophy and cardiac enlargement was found in CCH- but not in CIH-treated mouse heart. On one hand, upregulation in RNA and protein levels of eukaryotic translation initiation factor-2alpha and -4E (eIF-2alpha and eIF-4E) was found in CCH, whereas eIF-4E was downregulated in 1- and 2-wk CIH, suggesting that eIF-4E is likely to play an important role in the cardiac hypertrophy observed in CCH-treated mice. On the other hand, the specific downregulation of heart development-related genes (e.g., notch gene homolog-1, MAD homolog-4) and the upregulation of proteolysis genes (e.g., calpain-5) in the CIH heart can explain the lack of hypertrophy in CIH. Interestingly, apoptosis was enhanced in CCH but not CIH, and this was correlated with an upregulation of proapoptotic genes and downregulation of anti-apoptotic genes in CCH. In summary, our results indicate that 1) the pattern of gene response to CCH is different from that of CIH in mouse heart, and 2) the identified expression differences in certain gene groups are helpful in dissecting mechanisms responsible for phenotypes observed.
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Registered trials
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