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Updated: Feb 18, 2026
Induction of Hypoxia in Living Frog and Zebrafish Embryos
Published on: June 26, 2017
PHD in the FOXD1 lineage cells links hypoxia to inappropriate nephrogenesis
1Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan.
Abstract:
Insufficient oxygenation during pregnancy negatively influences kidney development, which likely serves as a predisposing factor in chronic kidney disease at later stages in life. In this issue of Kidney International, Kobayashi et al. demonstrate that deletion of prolyl hydroxylase 2 and 3, 2 of the major oxygen sensors, in the FoxD1 lineage cells reduces kidney size and inhibits nephrogenesis in mice. Temporospatial expression pattern and studies on additional knockouts suggest the involvement of hypoxia-inducible factor 2.
Insights
Pregnancy hypoxia impairs kidney development, increasing chronic kidney disease risk. Deleting oxygen sensors prolyl hydroxylase 2 and 3 in FoxD1 cells reduced kidney size and inhibited nephrogenesis in mice, implicating hypoxia-inducible factor 2.
Area of Science:
- Developmental biology
- Nephrology
- Oxygen sensing mechanisms
Background:
- Pregnancy hypoxia is linked to adverse kidney development.
- This may predispose individuals to chronic kidney disease later in life.
Purpose of the Study:
- To investigate the role of oxygen sensors in kidney development during pregnancy.
- To explore the impact of deleting specific oxygen sensors on nephrogenesis.
Main Methods:
- Deletion of prolyl hydroxylase 2 and 3 in FoxD1 lineage cells in mice.
- Analysis of kidney size and nephrogenesis.
- Temporospatial expression pattern analysis.
- Studies on additional knockout models.
Main Results:
- Deletion of prolyl hydroxylase 2 and 3 significantly reduced kidney size.
- Inhibition of nephrogenesis was observed in knockout mice.
- Hypoxia-inducible factor 2 was suggested to be involved.
Conclusions:
- Prolyl hydroxylase 2 and 3 play a critical role in kidney development.
- Oxygen sensing pathways, particularly involving hypoxia-inducible factor 2, are crucial for normal nephrogenesis.
- Understanding these mechanisms could inform strategies to mitigate risks associated with pregnancy hypoxia.
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