ArticleBiological research2025
NAMPT regulates mitochondria and oxidative stress level for mouse early embryo development.
Article in Biological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Significance of NAD anabolism profiles in neurological diseases.Metabolic brain disease · 2026Review
- Integrative multi-omics analysis of DNA methylome and transcriptome in a tyrosine kinase inhibitor LPM4870108-induced rat model of obesity.International journal of obesity (2005) · 2026Article
- Altered Embryonic SIRT6 and SIRT7 Expression Is Associated with Impaired Developmental Competence and Oocyte-Dependent Embryo Quality in Embryos Derived from Subfertile Males.International journal of molecular sciences · 2026Article
- Nicotinamide salvage is required for proliferation and sustaining self-renewal in undifferentiated embryonic stem cells.Stem cells (Dayton, Ohio) · 2026Article
- Transcriptomic Profiling of Peripheral Blood Identifies Candidate Genes for Early Pregnancy Diagnosis in Sika Deer.Animals : an open access journal from MDPI · 2025Article
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8 authors.
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Abstract
backgroundNicotinamide phosphoribosyltransferase (NAMPT) is an enzyme that involves into NMN-NAD + synthesis which involves into cellular metabolism related with aging, immune function, and neurodegeneration. However, its roles in early embryo development are still unclear.
methodsIn present study we disturbed the NAMPT activity and employed immunofluorescence staining and live cell imaging to explore its roles during early embryo development.
resultsWe showed that NAMPT mRNA level was stable during mouse early embryo development, and NAMPT accumulated in the nucleus of blastomeres in mouse embryos. The loss of NAMPT activity disturbed the early cleavage from zygote to 2-cell, 4-cell to morula formation in the dose-dependent manner. We found that NAMPT inhibition disrupted mitochondria function in 2-cell embryos, showing decreased mitochondria number and aberrant accumulation in the blastomeres, which further disturb mitochondrial membrane potential level and elevated ROS level in embryos, indicating the occurrence of oxidative stress. Moreover, NAMPT inhibition also increased the apoptotic index, showing with increased Annexin-V signals and apoptotic gene expression.
conclusionsTaken together, our study provided the evidence that NAMPT was essential for the mitochondria function to control oxidative stress and apoptosis during mouse early embryo development.
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