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Special Issue "Crosstalk between Circadian Rhythm and Diseases"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 November 2019.

Special Issue Editor

Dr. Fuyuki Sato
E-Mail Website
Guest Editor
Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan
Interests: crosstalk between circadian rhythm and tumor progression; pathological analysis in human and mouse tissues; functional analysis of DEC1 and DEC2 in tumor progression; molecular pathways of DEC1 and DEC2; crosstalk between basic and clinical research, involving clock genes
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Circadian rhythm is dominantly regulated by clock genes. Recent evidence suggests that the clock genes CLOCK, BMAL1/2, DEC1/2, PER1/2/3, and CRY1/2 play important roles in tumor progression, metabolism, immune responses, and sleep disorders by regulating apoptosis-related factors, cell cycle regulators, and inflammatory factors. On the other hand, various kinds of stress, such as hypoxia, inflammation, and anti-tumor drugs, affect the expression of clock genes. Therefore, clock genes have multiple functions in vivo that are associated with various kinds of diseases. Our aim is to improve the understanding of crosstalk between circadian rhythms, clock genes, and diseases to allow the development of strategies to overcome diseases, involving clock gene abnormalities. We encourage the submission of original articles and reviews involving circadian rhythm/clock genes and diseases.

Topics include, but are not limited to the following:

  • Relevant circadian rhythm/clock genes and diseases
  • Molecular pathways of clock genes, involving tumor progression, metabolism, inflammation, etc.
  • Functional analyses of clock genes in mouse models

The conjunct Special Issue in Clocks & Sleep: Crosstalk between Circadian Rhythm and Diseases

Dr. Fuyuki Sato
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • circadian rhythm
  • clock genes
  • tumor progression
  • metabolism
  • immune response
  • inflammation
  • molecular pathway

Published Papers (5 papers)

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Research

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Open AccessArticle
Circadian Gene Polymorphisms Associated with Breast Cancer Susceptibility
Int. J. Mol. Sci. 2019, 20(22), 5704; https://doi.org/10.3390/ijms20225704 - 14 Nov 2019
Abstract
Breast cancer (BC) is a major problem for civilization, manifested by continuously increasing morbidity and mortality among women worldwide. Core circadian genes may play an important role in cancer development and progression. To evaluate the effects of single nucleotide polymorphism (SNP) in circadian [...] Read more.
Breast cancer (BC) is a major problem for civilization, manifested by continuously increasing morbidity and mortality among women worldwide. Core circadian genes may play an important role in cancer development and progression. To evaluate the effects of single nucleotide polymorphism (SNP) in circadian genes in BC risk, 16 functional SNPs were genotyped in 321 BC patients and 364 healthy women using the TaqMan fluorescence-labelled probes or High-Resolution Melt Curve technique in the Real-Time PCR system. The selected SNPs were analyzed for the risk of BC, progression, and the influence on gene expression in BC tissue pairs to demonstrate the functionality of genetic variants. The study showed a relationship between an increased BC risk under the dominant genetic model of CRY2 rs10838524, PER2 rs934945, and recessive genetic model of PER1 rs2735611. A protective effect of BMAL1 rs2279287 was observed among carriers with at least one variant allele. Moreover, we found an increased risk of estrogen-/progesterone-positive tumors under the dominant genetic model of PER2 rs934945 and estrogen negative tumors under the variant genotype of CRY2 rs10838524, PER1 rs2735611. We demonstrated significantly altered gene expression of BMAL1, CRY2, PER1, PER2, PER3 according to particular genotypes in the BC tissue pairs. Our findings support the hypothesized role of circadian genes in breast carcinogenesis and indicate probable biomarkers for breast cancer susceptibility. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Open AccessArticle
The Mechanisms Underlying the Cytotoxic Effects of Copper Via Differentiated Embryonic Chondrocyte Gene 1
Int. J. Mol. Sci. 2019, 20(20), 5225; https://doi.org/10.3390/ijms20205225 - 22 Oct 2019
Abstract
Copper is an essential trace element within cells, but it also exerts cytotoxic effects through induction of reactive oxygen species (ROS) production. To determine the mechanisms underlying copper-induced ROS production, we examined the effects of copper sulfate in HeLa cells. Exposure to copper [...] Read more.
Copper is an essential trace element within cells, but it also exerts cytotoxic effects through induction of reactive oxygen species (ROS) production. To determine the mechanisms underlying copper-induced ROS production, we examined the effects of copper sulfate in HeLa cells. Exposure to copper sulfate led to dose-dependent decreases in HeLa cell viability, along with increases in the subG1 and G2/M populations and corresponding decreases in the G1 population. Copper sulfate also increased the levels of apoptosis, senescence, mitochondrial dysfunction, autophagy, ROS, and the expression of several stress proteins, including ATF3, c-Fos, DEC1 (differentiated embryonic chondrocyte gene 1), p21, p53, and HIF-1α (hypoxia-inducible factor 1 alpha). The suppression of copper-induced ROS generation by the ROS scavenger N-acetyl cysteine verified copper’s functional role, while the suppression of copper’s effects by the copper chelator disulfiram, confirmed its specificity. Selective induction of HIF-1α, p53, and phosphorylated ERK proteins by copper was blocked by the knockdown of the transcription factor DEC1, suggesting copper’s effects are mediated by DEC1. In addition to HeLa cells, copper also exerted cytotoxic effects in human endometrial (HEC-1-A) and lung (A549) adenocarcinoma cells, but not in normal human kidney (HEK293) or bronchial (Beas-2B) epithelial cells. These findings shed new light on the functional roles of copper within cells. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Open AccessArticle
Dec1 Deficiency Suppresses Cardiac Perivascular Fibrosis Induced by Transverse Aortic Constriction
Int. J. Mol. Sci. 2019, 20(19), 4967; https://doi.org/10.3390/ijms20194967 - 08 Oct 2019
Abstract
Cardiac fibrosis is a major cause of cardiac dysfunction in hypertrophic hearts. Differentiated embryonic chondrocyte gene 1 (Dec1), a basic helix–loop–helix transcription factor, has circadian expression in the heart; however, its role in cardiac diseases remains unknown. Therefore, using Dec1 knock-out [...] Read more.
Cardiac fibrosis is a major cause of cardiac dysfunction in hypertrophic hearts. Differentiated embryonic chondrocyte gene 1 (Dec1), a basic helix–loop–helix transcription factor, has circadian expression in the heart; however, its role in cardiac diseases remains unknown. Therefore, using Dec1 knock-out (Dec1KO) and wild-type (WT) mice, we evaluated cardiac function and morphology at one and four weeks after transverse aortic constriction (TAC) or sham surgery. We found that Dec1KO mice retained cardiac function until four weeks after TAC. Dec1KO mice also revealed more severely hypertrophic hearts than WT mice at four weeks after TAC, whereas no significant change was observed at one week. An increase in Dec1 expression was found in myocardial and stromal cells of TAC-treated WT mice. In addition, Dec1 circadian expression was disrupted in the heart of TAC-treated WT mice. Cardiac perivascular fibrosis was suppressed in TAC-treated Dec1KO mice, with positive immunostaining of S100 calcium binding protein A4 (S100A4), alpha smooth muscle actin (αSMA), transforming growth factor beta 1 (TGFβ1), phosphorylation of Smad family member 3 (pSmad3), tumor necrosis factor alpha (TNFα), and cyclin-interacting protein 1 (p21). Furthermore, Dec1 expression was increased in myocardial hypertrophy and myocardial infarction of autopsy cases. Taken together, our results indicate that Dec1 deficiency suppresses cardiac fibrosis, preserving cardiac function in hypertrophic hearts. We suggest that Dec1 could be a new therapeutic target in cardiac fibrosis. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Review

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Open AccessReview
Molecular Interactions between Pathogens and the Circadian Clock
Int. J. Mol. Sci. 2019, 20(23), 5824; https://doi.org/10.3390/ijms20235824 (registering DOI) - 20 Nov 2019
Abstract
The daily periodicity of the Earth’s rotation around the Sun, referred to as circadian (Latin “circa” = about, and “diem” = day), is also mirrored in the behavior and metabolism of living beings. The discovery that dedicated cellular genes control various aspects of [...] Read more.
The daily periodicity of the Earth’s rotation around the Sun, referred to as circadian (Latin “circa” = about, and “diem” = day), is also mirrored in the behavior and metabolism of living beings. The discovery that dedicated cellular genes control various aspects of this periodicity has led to studies of the molecular mechanism of the circadian response at the cellular level. It is now established that the circadian genes impact on a large network of hormonal, metabolic, and immunological pathways, affecting multiple aspects of biology. Recent studies have extended the role of the circadian system to the regulation of infection, host–pathogen interaction, and the resultant disease outcome. This critical review summarizes our current knowledge of circadian-pathogen interaction at both systemic and cellular levels, but with emphasis on the molecular aspects of the regulation. Wherever applicable, the potential of a direct interaction between circadian factors and pathogenic macromolecules is also explored. Finally, this review offers new directions and guidelines for future research in this area, which should facilitate progress. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Open AccessReview
The Role of the Molecular Clock in Promoting Skeletal Muscle Growth and Protecting against Sarcopenia
Int. J. Mol. Sci. 2019, 20(17), 4318; https://doi.org/10.3390/ijms20174318 - 03 Sep 2019
Abstract
The circadian clock has a critical role in many physiological functions of skeletal muscle and is essential to fully understand the precise underlying mechanisms involved in these complex interactions. The importance of circadian expression for structure, function and metabolism of skeletal muscle is [...] Read more.
The circadian clock has a critical role in many physiological functions of skeletal muscle and is essential to fully understand the precise underlying mechanisms involved in these complex interactions. The importance of circadian expression for structure, function and metabolism of skeletal muscle is clear when observing the muscle phenotype in models of molecular clock disruption. Presently, the maintenance of circadian rhythms is emerging as an important new factor in human health, with disruptions linked to ageing, as well as to the development of many chronic diseases, including sarcopenia. Therefore, the aim of this review is to present the latest findings demonstrating how circadian rhythms in skeletal muscle are important for maintenance of the cellular physiology, metabolism and function of skeletal muscle. Moreover, we will present the current knowledge about the tissue-specific functions of the molecular clock in skeletal muscle. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Author Name: Sato Fuyuki
Affiliation: Department of Pathology, Wakayama Medical University School of Medicine

Title: Crosstalk among circadian rhythm, obesity, and allergy
Authors: Kanami Orihara, et al.

Title: The emerging interplay between inflammation and the circadian clocks in metabolic disease
Authors: Eleonore Maury, et al.

Title: Disruption of dipping pattern of blood pressure is associated with the progression of renal injury during the development of salt-depending hypertension in rats
Authors: Asadur Rahman 1, Abu Sufiun 1, Kazi Rafiq 1, Yoshihide Fujisawa 2, Daisuke Nakano 1, Hideki Kobarai 3, Tsutomu Masaki 3 and Akira Nishiyama 1,*

Title: The role of clock genes in placenta
Authors: Xiaoyue Pan, et al.

Title: Molecular interactions between pathogens and the circadian clock
Authors: Sailen Barik, et al.

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