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Disturbed Diurnal Rhythm Alters Gene Expression and Exacerbates Cardiovascular Disease With Rescue by Resynchronization
Abstract
Day/night rhythms are recognized as important to normal cardiovascular physiology and timing of adverse cardiovascular events; however, their significance in disease has not been determined. We demonstrate that day/night rhythms play a critical role in compensatory remodeling of cardiovascular tissue, and disruption exacerbates disease pathophysiology. We use a murine model of pressure overload cardiac hypertrophy (transverse aortic constriction) in a rhythm-disruptive 20-hour versus 24-hour environment. Echocardiography reveals increased left ventricular end-systolic and -diastolic dimensions and reduced contractility in rhythm-disturbed transverse aortic constriction animals. Furthermore, cardiomyocytes and vascular smooth muscle cells exhibit reduced hypertrophy, despite increased pressure load. Microarray and real-time PCR demonstrate altered gene cycling in transverse aortic constriction myocardium and hypothalamic suprachiasmatic nucleus. With rhythm disturbance, there is a consequent altered cellular clock mechanism (per2 and bmal), whereas key genes in hypertrophic pathways (ANF, BNP, ACE, and collagen) are downregulated paradoxical to the increased pressure. Phenotypic rescue, including reversal/attenuation of abnormal pathology and genes, only occurs when the external rhythm is allowed to correspond with the animals' innate 24-hour internal rhythm. Our study establishes the importance of diurnal rhythm as a vital determinant in heart disease. Disrupted rhythms contribute to progression of organ dysfunction; restoration of normal diurnal schedules appears to be important for effective treatment of disease.
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“mice with surgically induced heart disease (cardiac hypertrophy through transverse aortic constriction) that live on an abnormal light/dark (10:10 h) cycle following surgery show impaired compensatory cardiac and vascular remodeling, reduced ventricular contractile strength, and increased blood pressure as compared to animals that live on a normal light/dark (12:12 h) cycle”
From The impact of the circadian timing system on cardiovascular and metabolic function (2012) · cites this paper as Martino et al., 2007
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“Phenotypic rescue, including reversal/attenuation of abnormal pathology and genes, only occurs when the external rhythm is allowed to correspond with the animals’ innate 24-h internal rhythm.”
From The impact of the circadian timing system on cardiovascular and metabolic function (2012) · cites this paper as Martino et al., 2007
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Metadata
- Authors
- Martino, T. A., Tata, N., Belsham, D. D., Chalmers, J., Straume, M., Lee, P., Pribiag, H., Khaper, N., Liu, P. P., Dawood, F., Backx, P. H., Ralph, M. R., & Sole, M. J.
- Affiliations
- University Health Network (CA)
- ORCID
- Venue
- Hypertension
- Published
- 2007-05
- Volume
- 49
- Issue
- 5
- Pages
- 1104-1113
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2148332803
- Cited by
- 196
- References
- 34
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 11 · 2023: 10 · 2022: 9 · 2021: 9 · 2020: 16 · 2019: 13 · 2018: 8 · 2017: 16 · 2016: 10 · 2015: 11 · 2014: 9 · 2013: 8 · 2012: 8
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- circadian rhythm, cardiac hypertrophy, pressure overload, transverse aortic constriction, gene expression, suprachiasmatic nucleus, clock genes, Per2, cardiomyocyte hypertrophy, vascular smooth muscle cells, left ventricular remodeling, atrial natriuretic peptide, brain natriuretic peptide, ACE, collagen, cardiovascular disease
- MeSH terms
- Animals, Biological Clocks, Brain, Circadian Rhythm, Echocardiography, Cardiomegaly, Hypertension, Male, Mice, Inbred C57BL, Myocardial Contraction, Myocardium, Severity of Illness Index, Gene Expression, Ventricular Remodeling, Gene Expression Profiling, Microarray Analysis, Mice
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