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<p>Irisin, a secreted myokine cleaved from FNDC5, regulates energy homeostasis and vascular function, but its role in pregnancy remains poorly understood. Here, using a murine model, we tested how global FNDC5 deficiency affects maternal metabolism, placental development and fetal growth, extending our earlier evidence that irisin mitigates human placental oxidative stress, reduces anti-angiogenic signaling and promotes trophoblast differentiation-factors involved in preeclampsia. Global FNDC5 knockout (KO) and wild-type (WT) mice were subjected to timed-mating and maternal, fetal and placental phenotypes were evaluated. Compared to WT, KO dams exhibited greater maternal body weight and a reduced fetal-to-placental weight ratio, while mean fetal and placental weights per litter were not significantly different. Knockout placentas showed reduced expression of labyrinth markers and glucose transporter gene, a trend toward reduced glycogen deposition at junctional zone, and altered CD31 expression-consistent with changes in placental architecture, nutrient transport, energy storage and utilization, and vasculature. Transcriptomic analyses comparing WT and KO placentas supported a role of irisin in placental and vascular development. Our findings indicate that irisin contributes to maternal weight regulation, fetal-placental interactions, and placental functional capacity. FNDC5 deficiency did not cause pregnancy failure but was associated with altered placental architecture and molecular markers relevant to exchange-surface development, highlighting FNDC5 as a potential modulator of late gestation placental phenotype and maternal-placental adaptation in pregnancy.</p>

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FNDC5 deficiency alters placental development, maternal body weight, and fetal-placental growth in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月25日

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  • Pinki Nandi,
  • Mavis Lee,
  • Dennis K. Lee,
  • Sascha Drewlo

摘要

Irisin, a secreted myokine cleaved from FNDC5, regulates energy homeostasis and vascular function, but its role in pregnancy remains poorly understood. Here, using a murine model, we tested how global FNDC5 deficiency affects maternal metabolism, placental development and fetal growth, extending our earlier evidence that irisin mitigates human placental oxidative stress, reduces anti-angiogenic signaling and promotes trophoblast differentiation-factors involved in preeclampsia. Global FNDC5 knockout (KO) and wild-type (WT) mice were subjected to timed-mating and maternal, fetal and placental phenotypes were evaluated. Compared to WT, KO dams exhibited greater maternal body weight and a reduced fetal-to-placental weight ratio, while mean fetal and placental weights per litter were not significantly different. Knockout placentas showed reduced expression of labyrinth markers and glucose transporter gene, a trend toward reduced glycogen deposition at junctional zone, and altered CD31 expression-consistent with changes in placental architecture, nutrient transport, energy storage and utilization, and vasculature. Transcriptomic analyses comparing WT and KO placentas supported a role of irisin in placental and vascular development. Our findings indicate that irisin contributes to maternal weight regulation, fetal-placental interactions, and placental functional capacity. FNDC5 deficiency did not cause pregnancy failure but was associated with altered placental architecture and molecular markers relevant to exchange-surface development, highlighting FNDC5 as a potential modulator of late gestation placental phenotype and maternal-placental adaptation in pregnancy.