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Inhibitor of DNA binding in heart development and cardiovascular diseases.

ABSTRACT: Id proteins, inhibitors of DNA binding, are transcription regulators containing a highly conserved helix-loop-helix domain. During multiple stages of normal cardiogenesis, Id proteins play major roles in early development and participate in the differentiation and proliferation of cardiac progenitor cells and mature cardiomyocytes. The fact that a depletion of Ids can cause a variety of defects in cardiac structure and conduction function is further evidence of their involvement in heart development. Multiple signalling pathways and growth factors are involved in the regulation of Ids in a cell- and tissue- specific manner to affect heart development. Recent studies have demonstrated that Ids are related to multiple aspects of cardiovascular diseases, including congenital structural, coronary heart disease, and arrhythmia. Although a growing body of research has elucidated the important role of Ids, no comprehensive review has previously compiled these scattered findings. Here, we introduce and summarize the roles of Id proteins in heart development, with the hope that this overview of key findings might shed light on the molecular basis of consequential cardiovascular diseases. Furthermore, we described the future prospective researches needed to enable advancement in the maintainance of the proliferative capacity of cardiomyocytes. Additionally, research focusing on increasing embryonic stem cell culture adaptability will help to improve the future therapeutic application of cardiac regeneration.

SUBMITTER: Hu W

PROVIDER: S-EPMC6534900 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Inhibitor of DNA binding in heart development and cardiovascular diseases.

Hu Wenyu W Xin Yanguo Y Hu Jian J Sun Yingxian Y Zhao Yinan Y

Cell communication and signaling : CCS 20190524 1

Id proteins, inhibitors of DNA binding, are transcription regulators containing a highly conserved helix-loop-helix domain. During multiple stages of normal cardiogenesis, Id proteins play major roles in early development and participate in the differentiation and proliferation of cardiac progenitor cells and mature cardiomyocytes. The fact that a depletion of Ids can cause a variety of defects in cardiac structure and conduction function is further evidence of their involvement in heart develop ...[more]

PMID: 31126344

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Project description:Congenital heart disease (CHD) is the most common life-threatening congenital anomaly. CHD occurs due to defects in cardiovascular development, and the majority of CHDs are caused by a multifactorial inheritance mechanism, which refers to the interaction between genetic and environmental factors. During embryogenesis, the cardiovascular system is derived from at least four distinct cell lineages: the first heart field, second heart field, cardiac neural crest, and proepicardial organ. Understanding the genes involved in each lineage is essential to uncover the genomic architecture of CHD. Therefore, we provide an overview of recent research progress using animal models and mutation analyses to better understand the molecular mechanisms and pathways linking cardiovascular development and CHD. For example, we highlight our recent work on genes encoding three isoforms of inositol 1,4,5-trisphosphate receptors (IP3R1, 2, and 3) that regulate various vital and developmental processes, which have genetic redundancy during cardiovascular development. Specifically, IP3R1 and 2 have redundant roles in the atrioventricular cushion derived from the first heart field lineage, whereas IP3R1 and 3 exhibit redundancy in the right ventricle and the outflow tract derived from the second heart field lineage, respectively. Moreover, 22q11.2 deletion syndrome (22q11DS) is highly associated with CHD involving the outflow tract, characterized by defects of the cardiac neural crest lineage. However, our studies have shown that TBX1, a major genetic determinant of 22q11DS, was not expressed in the cardiac neural crest but rather in the second heart field, suggesting the importance of the cellular interaction between the cardiac neural crest and the second heart field. Comprehensive genetic analysis using the Japanese genome bank of CHD and mouse models revealed that a molecular regulatory network involving GATA6, FOXC1/2, TBX1, SEMA3C, and FGF8 was essential for reciprocal signaling between the cardiac neural crest and the second heart field during cardiovascular development. Elucidation of the genomic architecture of CHD using induced pluripotent stem cells and next-generation sequencing technology, in addition to genetically modified animal models and human mutation analyses, would facilitate the development of regenerative medicine and/or preventive medicine for CHD in the near future.

Project description:IntroductionCardiovascular diseases (CVDs) are the number one cause of death, and there is evidence that work exposures could be associated with their development. This study aimed to systematically review observational studies of adults exposed to job strain, effort-reward imbalance, long working hours, job insecurity, shift work, and occupational noise, and assess the association of those work exposures with CVDs.MethodsThe Navigation Guide framework was applied. The population were adults of working age (18-65), and cohort and case-control studies were included. The work exposures were job strain, effort-reward imbalance, long working hours, job insecurity, shift work, and occupational noise. The outcomes were cerebrovascular diseases, ischaemic heart disease, and hypertensive diseases. The selection, data extraction, risk of bias assessment, and quality assessment were carried out by two reviewers independently and disagreements were solved by a third reviewer or by consensus. The synthesis of the results was done by applying the 'vote counting based on direction' method, and the results were summarized in an effect direction plot. The strength of the evidence for every risk factor and CVD was defined by consensus.ResultsA total of 17 643 papers were initially identified in the literature search, but after applying the filters by title and abstract, and full text, 86 studies were finally included. From the included studies, sufficient evidence was found of the harmfulness of job strain for cerebrovascular disease and ischemic heart disease. Furthermore, there was sufficient evidence of the harmfulness of shift work for ischemic heart disease. Evidence of no relationship was found between long working hours and shift work with ischaemic heart disease and hypertensive disease, respectively. The other associations of work exposures and CVDs had limited or inadequate evidence of harmfulness.ConclusionsIn this comprehensive review, there was sufficient evidence of a harmful relationship between job strain, shift work, and CVDs. For the other work exposures, more high-quality studies are needed. In order to improve current prevention strategies for CVDs, the findings of this review imply that job strain and shift work are work exposures that constitute additional risk factors that could be approached as targets for worksite interventions.Systematic review registrationPROSPERO CRD42020179972.

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Inhibitor of DNA binding in heart development and cardiovascular diseases.

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Inhibitor of DNA binding in heart development and cardiovascular diseases.

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