What is it about?

Kidney development ceases at the end of the third trimester of pregnancy, with no new nephrons forming after birth even with numerous injuries. Therefore, the intrauterine environment, as the maternal nutritional state, has a high effect on the risk of kidney disease when the fetus reaches adulthood. Impairment of mTOR pathway activity and methionine metabolism in nephron progenitor cells play a pivotal role in mediating the effect of caloric restriction during pregnancy on nephron endowment in a mouse model. Increasing the activity of the mTOR pathway or methionine supplementation during pregnancy reverses the negative effect of maternal malnutrition on the developing kidney.

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Why is it important?

These results highlight new interventions to improve nephrogenesis in high-risk pregnancies.

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This page is a summary of: Increasing mTORC1 Pathway Activity or Methionine Supplementation during Pregnancy Reverses the Negative Effect of Maternal Malnutrition on the Developing Kidney, Journal of the American Society of Nephrology, May 2021, American Society of Nephrology, DOI: 10.1681/asn.2020091321.
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