Environmental Alterations during Embryonic Development: Studying the Impact of Stressors on Pluripotent Stem Cell-Derived Cardiomyocytes.
Federica LambertoIrene Peral-SanchezSuchitra MuenthaisongMelinda ZanaSandrine Willaime-MorawekAndrás DinnyésPublished in: Genes (2021)
Non-communicable diseases (NCDs) sauch as diabetes, obesity and cardiovascular diseases are rising rapidly in all countries world-wide. Environmental maternal factors (e.g., diet, oxidative stress, drugs and many others), maternal illnesses and other stressors can predispose the newborn to develop diseases during different stages of life. The connection between environmental factors and NCDs was formulated by David Barker and colleagues as the Developmental Origins of Health and Disease (DOHaD) hypothesis. In this review, we describe the DOHaD concept and the effects of several environmental stressors on the health of the progeny, providing both animal and human evidence. We focus on cardiovascular diseases which represent the leading cause of death worldwide. The purpose of this review is to discuss how in vitro studies with pluripotent stem cells (PSCs), such as embryonic and induced pluripotent stem cells (ESC, iPSC), can underpin the research on non-genetic heart conditions. The PSCs could provide a tool to recapitulate aspects of embryonic development "in a dish", studying the effects of environmental exposure during cardiomyocyte (CM) differentiation and maturation, establishing a link to molecular mechanism and epigenetics.
Keyphrases
- induced pluripotent stem cells
- cardiovascular disease
- human health
- pluripotent stem cells
- oxidative stress
- healthcare
- public health
- type diabetes
- life cycle
- weight loss
- mental health
- risk assessment
- endothelial cells
- metabolic syndrome
- insulin resistance
- heart failure
- birth weight
- genome wide
- dna damage
- dna methylation
- weight gain
- signaling pathway
- gene expression
- glycemic control
- ischemia reperfusion injury
- cardiovascular events
- copy number
- physical activity
- angiotensin ii
- skeletal muscle
- coronary artery disease
- induced apoptosis
- high glucose