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Updated: Apr 4, 2026
Using Chicken Embryo as a Powerful Tool in Assessment of Developmental Cardiotoxicities
Published on: March 21, 2021
The impact of high-salt exposure on cardiovascular development in the early chick embryo
Guang Wang1, Nuan Zhang1, Yi-Fan Wei1
1Key Laboratory for Regenerative Medicine of the Ministry of Education, Division of Histology and Embryology, Medical College, Jinan University, Guangzhou 510632, China.
Insights
High salt intake during embryonic development significantly increases chick mortality by impairing heart formation and blood vessel development. Excess reactive oxygen species (ROS) appear to be a key factor in these salt-induced developmental defects.
Area of Science:
- Developmental biology
- Cardiovascular physiology
- Toxicology
Background:
- Embryonic mortality is often linked to cardiovascular developmental issues.
- High-salt environments can pose risks to developing organisms.
Purpose of the Study:
- To investigate the impact of high-salt exposure on early embryonic development in chicks.
- To identify the mechanisms underlying salt-induced cardiovascular and angiogenic defects.
Main Methods:
- Exposure of chick embryos to high-salt conditions.
- Analysis of heart development, including looping and cell proliferation/apoptosis.
- Assessment of angiogenesis in yolk sac membrane (YSM) and chorioallantoic membrane models.
- Gene expression analysis (Nkx2.5, GATA4, HIF2, FGF2).
- Measurement of reactive oxygen species (ROS) generation.
Main Results:
- High salt significantly increased embryonic mortality and caused heart tube looping defects and blood congestion.
- Ventricular cell proliferation and apoptosis increased under high-salt conditions, leading to incomplete differentiation.
- Angiogenesis was suppressed, with reduced blood vessel density and diameter, and inhibited blood island formation.
- High salt led to increased ROS generation in cardiac and YSM tissues, which was partially ameliorated by antioxidants.
Conclusions:
- High-salt exposure severely impacts chick embryonic cardiovascular development and angiogenesis.
- Incomplete differentiation, altered cell proliferation/apoptosis, and suppressed angiogenesis are key salt-induced defects.
- Excess ROS generation is implicated as a major contributor to high-salt-induced developmental abnormalities.
Abstract:
In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-salt-suppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-salt-induced defects in heart and angiogenesis.
