Mending a broken heart: In vitro , in vivo and in silico models of congenital heart disease

Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are...

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Published inDisease models & mechanisms Vol. 14; no. 3
Main Authors Rufaihah, Abdul Jalil, Chen, Ching Kit, Yap, Choon Hwai, Mattar, Citra N. Z.
Format Journal Article
LanguageEnglish
Published England The Company of Biologists Ltd 28.03.2021
The Company of Biologists
Subjects
animal models
Animals
biomechanics
cardiogenesis
Cardiovascular disease
Cell adhesion & migration
Computer Simulation
Congenital diseases
congenital heart disease
Coronary vessels
Defects
Disease Models, Animal
Epigenesis, Genetic
Fetuses
Gene expression
Heart
Heart - embryology
Heart - physiopathology
Heart Defects, Congenital - genetics
Heart Defects, Congenital - pathology
Heart Defects, Congenital - physiopathology
Humans
Mechanical properties
Pulmonary arteries
Regeneration
Review
shear wall stresses
structural anomalies
Transcription factors
Veins & arteries
Biomechanics
Structural anomalies
Animal models
Congenital heart disease
Cardiogenesis
Shear wall stresses
Online AccessGet full text
ISSN1754-8403
1754-8411
1754-8411
DOI10.1242/dmm.047522

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Abstract Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are palliative at best. For this reason, the complex process of cardiogenesis, governed by multiple interlinked and dose-dependent pathways, is well investigated. Tissue, animal and, more recently, computerized models of the developing heart have facilitated important discoveries that are helping us to understand the genetic, epigenetic and mechanobiological contributors to CHD aetiology. In this Review, we discuss the strengths and limitations of different models of normal and abnormal cardiogenesis, ranging from single-cell systems and 3D cardiac organoids, to small and large animals and organ-level computational models. These investigative tools have revealed a diversity of pathogenic mechanisms that contribute to CHD, including genetic pathways, epigenetic regulators and shear wall stresses, paving the way for new strategies for screening and non-surgical treatment of CHD. As we discuss in this Review, one of the most-valuable advances in recent years has been the creation of highly personalized platforms with which to study individual diseases in clinically relevant settings.
AbstractList Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are palliative at best. For this reason, the complex process of cardiogenesis, governed by multiple interlinked and dose-dependent pathways, is well investigated. Tissue, animal and, more recently, computerized models of the developing heart have facilitated important discoveries that are helping us to understand the genetic, epigenetic and mechanobiological contributors to CHD aetiology. In this Review, we discuss the strengths and limitations of different models of normal and abnormal cardiogenesis, ranging from single-cell systems and 3D cardiac organoids, to small and large animals and organ-level computational models. These investigative tools have revealed a diversity of pathogenic mechanisms that contribute to CHD, including genetic pathways, epigenetic regulators and shear wall stresses, paving the way for new strategies for screening and non-surgical treatment of CHD. As we discuss in this Review, one of the most-valuable advances in recent years has been the creation of highly personalized platforms with which to study individual diseases in clinically relevant settings.
Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are palliative at best. For this reason, the complex process of cardiogenesis, governed by multiple interlinked and dose-dependent pathways, is well investigated. Tissue, animal and, more recently, computerized models of the developing heart have facilitated important discoveries that are helping us to understand the genetic, epigenetic and mechanobiological contributors to CHD aetiology. In this Review, we discuss the strengths and limitations of different models of normal and abnormal cardiogenesis, ranging from single-cell systems and 3D cardiac organoids, to small and large animals and organ-level computational models. These investigative tools have revealed a diversity of pathogenic mechanisms that contribute to CHD, including genetic pathways, epigenetic regulators and shear wall stresses, paving the way for new strategies for screening and non-surgical treatment of CHD. As we discuss in this Review, one of the most-valuable advances in recent years has been the creation of highly personalized platforms with which to study individual diseases in clinically relevant settings. Summary: In vitro , in vivo and in silico models of congenital heart disease provide important insights into the causes, evolution and pathological effects of congenital structural heart disease – a group of largely heterogenous disorders with substantial morbidity – and aid in designing effective therapies.
Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are palliative at best. For this reason, the complex process of cardiogenesis, governed by multiple interlinked and dose-dependent pathways, is well investigated. Tissue, animal and, more recently, computerized models of the developing heart have facilitated important discoveries that are helping us to understand the genetic, epigenetic and mechanobiological contributors to CHD aetiology. In this Review, we discuss the strengths and limitations of different models of normal and abnormal cardiogenesis, ranging from single-cell systems and 3D cardiac organoids, to small and large animals and organ-level computational models. These investigative tools have revealed a diversity of pathogenic mechanisms that contribute to CHD, including genetic pathways, epigenetic regulators and shear wall stresses, paving the way for new strategies for screening and non-surgical treatment of CHD. As we discuss in this Review, one of the most-valuable advances in recent years has been the creation of highly personalized platforms with which to study individual diseases in clinically relevant settings.Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect among newborns worldwide. Despite the significant impact on human health, most treatments available for this heterogenous group of disorders are palliative at best. For this reason, the complex process of cardiogenesis, governed by multiple interlinked and dose-dependent pathways, is well investigated. Tissue, animal and, more recently, computerized models of the developing heart have facilitated important discoveries that are helping us to understand the genetic, epigenetic and mechanobiological contributors to CHD aetiology. In this Review, we discuss the strengths and limitations of different models of normal and abnormal cardiogenesis, ranging from single-cell systems and 3D cardiac organoids, to small and large animals and organ-level computational models. These investigative tools have revealed a diversity of pathogenic mechanisms that contribute to CHD, including genetic pathways, epigenetic regulators and shear wall stresses, paving the way for new strategies for screening and non-surgical treatment of CHD. As we discuss in this Review, one of the most-valuable advances in recent years has been the creation of highly personalized platforms with which to study individual diseases in clinically relevant settings.
Author Mattar, Citra N. Z.
Yap, Choon Hwai
Chen, Ching Kit
Rufaihah, Abdul Jalil
AuthorAffiliation 4 Division of Cardiology, Department of Paediatrics, Khoo Teck Puat -National University Children's Medical Institute, National University Health System , Singapore 119228
6 Experimental Fetal Medicine Group, Department of Obstetrics and Gynaecology , Yong Loo Lin School of Medicine, National University of Singapore , Singapore 119228
7 Department of Obstetrics and Gynaecology , National University Health System , Singapore 119228
5 Department of Bioengineering , Imperial College London , London , UK
3 Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
1 Healthy Longevity Translational Research Programme , Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
2 Department of Surgery , Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
AuthorAffiliation_xml – name: 1 Healthy Longevity Translational Research Programme , Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
– name: 4 Division of Cardiology, Department of Paediatrics, Khoo Teck Puat -National University Children's Medical Institute, National University Health System , Singapore 119228
– name: 5 Department of Bioengineering , Imperial College London , London , UK
– name: 6 Experimental Fetal Medicine Group, Department of Obstetrics and Gynaecology , Yong Loo Lin School of Medicine, National University of Singapore , Singapore 119228
– name: 7 Department of Obstetrics and Gynaecology , National University Health System , Singapore 119228
– name: 2 Department of Surgery , Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
– name: 3 Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore , Singapore, 119228
Author_xml – sequence: 1
  givenname: Abdul Jalil
  orcidid: 0000-0002-9764-8668
  surname: Rufaihah
  fullname: Rufaihah, Abdul Jalil
  organization: Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 119228
– sequence: 2
  givenname: Ching Kit
  orcidid: 0000-0003-4302-3539
  surname: Chen
  fullname: Chen, Ching Kit
  organization: Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 119228, Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 119228
– sequence: 3
  givenname: Choon Hwai
  orcidid: 0000-0003-2918-3077
  surname: Yap
  fullname: Yap, Choon Hwai
  organization: Division of Cardiology, Department of Paediatrics, Khoo Teck Puat -National University Children's Medical Institute, National University Health System, Singapore 119228, Department of Bioengineering, Imperial College London, London, UK
– sequence: 4
  givenname: Citra N. Z.
  orcidid: 0000-0003-0068-6957
  surname: Mattar
  fullname: Mattar, Citra N. Z.
  organization: Experimental Fetal Medicine Group, Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Department of Obstetrics and Gynaecology, National University Health System, Singapore 119228
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33787508$$D View this record in MEDLINE/PubMed
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Keywords Biomechanics
Structural anomalies
Animal models
Congenital heart disease
Cardiogenesis
Shear wall stresses
Language English
License http://creativecommons.org/licenses/by/4.0
2021. Published by The Company of Biologists Ltd.
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Snippet Birth defects contribute to ∼0.3% of global infant mortality in the first month of life, and congenital heart disease (CHD) is the most common birth defect...
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SubjectTerms animal models
Animals
biomechanics
cardiogenesis
Cardiovascular disease
Cell adhesion & migration
Computer Simulation
Congenital diseases
congenital heart disease
Coronary vessels
Defects
Disease Models, Animal
Epigenesis, Genetic
Fetuses
Gene expression
Heart
Heart - embryology
Heart - physiopathology
Heart Defects, Congenital - genetics
Heart Defects, Congenital - pathology
Heart Defects, Congenital - physiopathology
Humans
Mechanical properties
Pulmonary arteries
Regeneration
Review
shear wall stresses
structural anomalies
Transcription factors
Veins & arteries
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Title Mending a broken heart: In vitro , in vivo and in silico models of congenital heart disease
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Volume 14
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