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      Sympathetic Nervous System Mediates Cardiac Remodeling After Myocardial Infarction in a Circadian Disruption Model

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          Abstract

          Background: Circadian rhythms have a considerable impact on the daily physiology of the heart, and their disruption causes pathology. Several studies have revealed that circadian disruption impaired cardiac remodeling after myocardial infarction (MI); however, the underlying brain-heart mechanisms remain unknown. We aim to discuss whether circadian disruption facilitates cardiac remodeling after MI by activating sympathetic nervous system.

          Methods: Rats were randomly divided into three groups: Sham group (Sham), MI group (MI), and MI+ circadian disruption group (MI+Dis); rats were treated with pseudorabies virus (PRV) injections for trans-synaptic retrograde tracing; rats were randomly divided into two groups: MI+ circadian disruption + Empty Vector+ clozapine N-oxide (CNO) (Empty Vector), and MI+ circadian disruption + hM4D(Gi)+ CNO [hM4D(Gi)].

          Results: Circadian disruption significantly facilitated cardiac remodeling after MI with lower systolic function, larger left ventricular volume, and aggravated cardiac fibrosis. Cardiac sympathetic remodeling makers and serum norepinephrine levels were also significantly increased by circadian disruption. PRV virus-labeled neurons were identified in the superior cervical ganglion (SCG), paraventricular nucleus (PVN), and suprachiasmatic nucleus (SCN) regions. Ganglionic blockade via designer receptors exclusively activated by designer drugs (DREADD) technique suppressed the activity of sympathetic nervous system and significantly alleviated the disruption-related cardiac dysfunction.

          Conclusion: Circadian disruption adversely affected cardiac remodeling after MI possibly by activating sympathetic nervous system, and suppressing sympathetic activity can attenuate this disruption-related cardiac dysfunction.

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          Obesity and metabolic syndrome in circadian Clock mutant mice.

          Fred Turek, Corinne Joshu, Akira Kohsaka … (2005)
          The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.
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            IL-18 cleavage triggers cardiac inflammation and fibrosis upon β-adrenergic insult.

            Han Xiao, Hao Li, Jing-Jing Wang … (2017)
            Rapid over-activation of β-adrenergic receptor (β-AR) upon stress leads to cardiac inflammation, a prevailing factor that underlies heart injury. However, mechanisms by which acute β-AR stimulation induce cardiac inflammation still remain unknown. Here, we set out to identify the crucial role of inflammasome/interleukin (IL)-18 in initiating and maintaining cardiac inflammatory cascades upon β-AR insult.
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              Insomnia and the risk of acute myocardial infarction: a population study.

              Carl G P Platou, L. J. Vatten, Imre Janszky … (2011)
              Few prospective studies have investigated insomnia in relation to risk for coronary heart disease. We assessed insomnia symptoms and risk of acute myocardial infarction (AMI) in a large, population-based study. A total of 52 610 men and women were followed up for a first AMI, and 2368 incident AMIs occurred during 11.4 years of follow-up, either identified at hospitals or by the National Cause of Death Registry. In our analyses, we adjusted for age, sex, marital status, education, shift work, blood pressure, lipids, diabetes mellitus, body mass index, physical activity, smoking, and alcohol consumption. Difficulties initiating and maintaining sleep and having a feeling of nonrestorative sleep were associated with a moderate increase in AMI risk. The multiadjusted hazard ratios for AMI were 1.45 (95% confidence interval 1.18-1.80) for people with difficulties initiating sleep almost every night, 1.30 (1.01-1.68) for those with difficulties maintaining sleep almost every night, and 1.27 (1.03-1.57) for those with a feeling of nonrestorative sleep more than once a week compared with people who never experienced these sleep difficulties. When we combined the symptoms, a dose-dependent association was seen between the number of insomnia symptoms and AMI risk (P for trend 0.003). Alternative multivariable models and different sensitivity analyses suggest that the results were robust, especially concerning difficulties initiating sleep. Insomnia is associated with a moderately increased risk for AMI.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Cardiovasc Med
                Journal ID (iso-abbrev): Front Cardiovasc Med
                Journal ID (publisher-id): Front. Cardiovasc. Med.
                Title: Frontiers in Cardiovascular Medicine
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 2297-055X
                Publication date (Electronic): 26 March 2021
                Publication date Collection: 2021
                Volume: 8
                Electronic Location Identifier: 668387
                Affiliations
                [1] 1Department of Cardiology, Renmin Hospital of Wuhan University , Wuhan, China
                [2] 2Cardiac Autonomic Nervous Research Center, Wuhan University , Wuhan, China
                [3] 3Department of Cardiology Cardiovascular Research Institute, Wuhan University , Wuhan, China
                [4] 4Hubei Key Laboratory of Cardiology , Wuhan, China
                [5] 5Department of Thoracic Surgery, Renmin Hospital of Wuhan University , Wuhan, China
                Author notes

                Edited by: Jinwei Tian, The Second Affiliated Hospital of Harbin Medical University, China

                Reviewed by: Jianyun Yan, Southern Medical University, China; Dachun Xu, Tongji University, China

                *Correspondence: Hong Jiang hong-jiang@ 123456whu.edu.cn

                This article was submitted to General Cardiovascular Medicine, a section of the journal Frontiers in Cardiovascular Medicine

                †These authors have contributed equally to this work

                Article
                DOI: 10.3389/fcvm.2021.668387
                PMC ID: 8032890
                PubMed ID: 33842566
                SO-VID: d14dde29-b0e1-4534-ab1b-af3a33004bb2
                Copyright © Copyright © 2021 Wang, Jiang, Chen, Zhou, Liu, Liu, Liu, Zhou, Zhou, Yu and Jiang.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 16 February 2021
                Date accepted : 04 March 2021
                Page count
                Figures: 6, Tables: 0, Equations: 0, References: 41, Pages: 11, Words: 6000
                Categories
                Subject: Cardiovascular Medicine
                Subject: Original Research

                Keywords: sympathetic nervous system,autonomic nervous system,cardiac dysfunction,circadian disruption,sympathetic ganglionic blockade
                Data availability:
                Keywords: sympathetic nervous system, autonomic nervous system, cardiac dysfunction, circadian disruption, sympathetic ganglionic blockade

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