Please use this identifier to cite or link to this item: https://doi.org/10.1242/dmm.047522
Title: Mending a broken heart: In vitro, in vivo and in silico models of congenital heart disease
Authors: Rufaihah, Abdul Jalil 
Chen, Ching Kit 
Yap, Choon Hwai
Mattar, Citra NZ 
Keywords: Science & Technology
Life Sciences & Biomedicine
Cell Biology
Pathology
KEY WORDS
Animal models
Biomechanics
Cardiogenesis
Congenital heart disease
Shear wall stresses
Structural anomalies
PLURIPOTENT STEM-CELLS
CARDIAC NEURAL CREST
VENTRICULAR SEPTAL-DEFECTS
DE-NOVO MUTATIONS
COMPARATIVE GENOMIC HYBRIDIZATION
COMPUTATIONAL FLUID-DYNAMICS
HELIX TRANSCRIPTION FACTORS
T-BOX GENES
OUTFLOW-TRACT
CARDIOVASCULAR DEVELOPMENT
Issue Date: 1-Mar-2021
Publisher: COMPANY BIOLOGISTS LTD
Citation: Rufaihah, Abdul Jalil, Chen, Ching Kit, Yap, Choon Hwai, Mattar, Citra NZ (2021-03-01). Mending a broken heart: In vitro, in vivo and in silico models of congenital heart disease. DISEASE MODELS & MECHANISMS 14 (3). ScholarBank@NUS Repository. https://doi.org/10.1242/dmm.047522
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 nonsurgical 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.
Source Title: DISEASE MODELS & MECHANISMS
URI: https://scholarbank.nus.edu.sg/handle/10635/191443
ISSN: 17548403
17548411
DOI: 10.1242/dmm.047522
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