ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The Placenta Regulates Intrauterine Fetal Growth via Exosomal PPARγ.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- Maternal obesity programs offspring metabolic dysfunction via small extracellular vesicle-mediated epigenetic remodeling.Nature communications · 2026Article
- PMOS in black girls and women: from high to low risk.Journal of endocrinological investigation · 2026Article
- Placenta-Derived Extracellular Vesicles (pdEVs): Key Mediators That Affect the Metabolic Health of Offspring in Early Nutritional Environments.Biomolecules · 2026Review
- Understanding Intracellular Transport Impairments in Maternal Protein Restriction: A Scoping Review of DOHaD-Driven Cellular Biology Perspective.Cell biochemistry and biophysics · 2026Article
- The Role of Exosomes in Offspring Metabolic Programming in Gestational Diabetes: Mechanisms and Potential Applications.International journal of biological sciences · 2026Review
- Exosome-Based Therapies for Skin Aging: Sources, Mechanisms, and Evidence from Preclinical and Clinical Studies.International journal of nanomedicine · 2026Review
- Crosstalk of extracellular vesicles in maternal-fetal interaction.Frontiers in cell and developmental biology · 2026Review
- Serum physiology, fecal microbiota, and metabolome signatures associated with perinatal stage transitions in Mongolian mares.Frontiers in veterinary science · 2026Article
- Folic acid ameliorates placental structure and function in fetal growth restriction via epigenetic modifications.Clinical epigenetics · 2025Article
- The Placenta Regulates Intrauterine Fetal Growth via Exosomal PPARγ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Comparative analysis of lipid metabolism in trophoblast subpopulations in preeclampsia andFrontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Abnormal adipogenesis is a major contributor to fetal growth restriction (FGR) and its associated complications. However, the underlying etiology remains unclear. Here, it is reported that the placentas of women with pregnancies complicated with FGR exhibit peroxisome proliferator-activated receptor γ (PPARγ) inactivation. In mice, trophoblast-specific ablation of murine PPARγ reproduces the phenotype of human fetuses with FGR and defective adipogenesis. Coculture of trophoblasts with preadipocytes significantly improves preadipocyte commitment and differentiation and increases the transcription of a series of adipogenic genes via intercellular transfer of exosomal PPARγ proteins. Moreover, nanoparticle-mediated placenta-specific delivery of rosiglitazone (RGZ) significantly rescues adipogenesis defects in an FGR-induced mouse model. In summary, the placenta is a major reservoir of PPARγ. An insufficient supply of placental PPARγ to fetal preadipocytes via exosomes during late gestation is a major mechanism underlying FGR. Preclinically, placenta-targeted RGZ administration can be a promising interventional therapy for FGR and/or defective intrauterine fat development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.