ArticleNucleic acids research2025
Lactylation of CREB is required for FSH-induced proliferation and differentiation of ovarian granulosa cells.
Article in Nucleic acids research, 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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Who cites it
11 citing papers in PubMed.
- HSP90α lactylation orchestrates PGC1α and LRPGC1 nuclear translocation driving mitochondrial biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- Article
- Mechanism and Intervention of the NPY1R/CREB Signaling Axis in Regulating Inflammatory Response in Aged Ovarian Granulosa Cells and Ovarian Senescence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- FOXK1: a multifaceted regulator in metabolic reprogramming and disease progression.Biology direct · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Dysregulated post‑translational modifications in granulosa cells drive ovarian dysfunction and potential infertility applications (Review).International journal of molecular medicine · 2026Review
- ANGPT2/Tie2 Enhances H3K18la-Mediated Macrophage M2 Polarization to Promote Endothelial Cell Proliferation in the Chronically Ischaemic Brain.CNS neuroscience & therapeutics · 2026Article
- Beyond a metabolite: lactate and lactylation in lung diseases.Respiratory research · 2026Review
- Histone Lactylation Couples FSH-Driven Lactate Metabolism to Mitochondrial Biogenesis by Enhancing HDAC4-Mediated Deacetylation of PGC-1α in Granulosa Cells.Research (Washington, D.C.) · 2026Article
- Research progress on protein lactylation in female reproductive disease: molecular mechanisms, functions, and therapeutic implications.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Follicle-stimulating hormone (FSH) promotes follicular development by inducing the proliferation and differentiation of granulosa cells (GCs). This process is primarily attributed to the activation of the canonical G protein-coupled receptor (GPCR)/adenylyl cyclase/cAMP/PKA/CREB signaling pathway. Here, we revealed a novel mechanism wherein FSH promotes GCs proliferation and differentiation by stimulating cAMP response element-binding protein (CREB) lactylation. Specifically, FSH induced CREB lactylation at lysine 136 (K136la), leading to CREB phosphorylation at serine 133, which facilitated CREB/CBP/P300 complex formation for transcription activation. Moreover, K136la alone directly recruited CBP/P300, triggering transcriptional surges of proliferation and differentiation genes by binding with the cAMP response element (CRE), thereby stimulating GCs proliferation and differentiation. By contrast, a CREB mutation at K136 eliminated these effects. Blocking CREB lactylation using oxamate or C646 in vivo suppressed GCs proliferation, differentiation, and follicular development in mouse ovaries. These findings highlight the important role of lactylation between metabolic regulation and folliculogenesis, and its importance in mediating GPCR signaling, providing a theoretical basis for treating female infertility associated with defective follicular development.
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Registered trials
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