Cited by 196Circadian rhythm and melatoninCardiac electrophysiology and arrhythmiasCardiac Fibrosis and Remodeling

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Disturbed Diurnal Rhythm Alters Gene Expression and Exacerbates Cardiovascular Disease With Rescue by Resynchronization

Martino, Tami A., Tata, Nazneen, Belsham, Denise D., Chalmers, Jennifer, Straume, Marty, Lee, Paul, Pribiag, Horia, Khaper, Neelam, Liu, Peter P., Dawood, Fayez, Backx, Peter H., Ralph, Martin R., Sole, Michael J.·2007·Hypertension

DOI 10.1161/hypertensionaha.106.083568

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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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10.1161/circ.79.4.2647318 · DOI
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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: Martino, Tami A.
Belsham, Denise D.
Lee, Paul
Pribiag, Horia
Khaper, Neelam
Liu, Peter P.
Backx, Peter H.
Ralph, Martin R.
Venue: Hypertension
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2007-05
Volume: 49
Issue: 5
Pages: 1104-1113
ISSN: 0194-911X (ISSN-L)
1524-4563
DOI: 10.1161/hypertensionaha.106.083568
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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Disturbed Diurnal Rhythm Alters Gene Expression and Exacerbates Cardiovascular Disease With Rescue by Resynchronization

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