ArticleCell death & disease2021
hPER3 promotes adipogenesis via hHSP90AA1-mediated inhibition of Notch1 pathway.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Shift work disrupts Immune regulation of the transcriptome in hospital nurses.Frontiers in public health · 2026Article
- NAT10-mediated N4-acetylcytidine modification in KLF9 mRNA promotes adipogenesis.Cell death and differentiation · 2025Article
- Genetic variation in NOTCH1 is associated with overweight and obesity in Brazilian elderly.Scientific reports · 2024Article
- Revealing Molecular Mechanisms of the Bioactive Saponins from Edible Root ofPlants (Basel, Switzerland) · 2024Article
- Shift work promotes adipogenesis via cortisol-dependent downregulation of EGR3-HDAC6 pathway.Cell death discovery · 2024Article
- Characteristics of insulin resistance in Korean adults from the perspective of circadian and metabolic sensing genes.Genes & genomics · 2023Article
- Ginsenoside Rk1 inhibits HeLa cell proliferation through an endoplasmic reticulum signaling pathway.Journal of ginseng research · 2023Article
- HSF1 Alleviates Brain Injury by Inhibiting NLRP3-Induced Pyroptosis in a Sepsis Model.Mediators of inflammation · 2023Article
- Stem Cell Transplantation in the Treatment of Type 1 Diabetes Mellitus: From Insulin Replacement to Beta-Cell Replacement.Frontiers in endocrinology · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The period circadian regulator 3 (PER3) has been reported to play a negative role in human immortalized bone marrow-derived Scp-1 cells (iBMSCs) and patient adipose-derived stromal cells (PASCs) or a negative/positive role in mice adipogenesis. However, human PER3 (hPER3) was identified as a positive regulator of human adipose tissue-derived stromal cells (hADSCs) adipogenesis in this study. Silencing or overexpression of hPER3 in hADSCs inhibited and promoted adipogenesis in vitro. In vivo, the overexpression of hPER3 increased high-fat diet-induced inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) forms, increasing systemic glucose intolerance and insulin resistance. Molecularly, hPER3 does not interact with hPPARγ, but represses Notch1 signaling pathway to enhance adipogenesis by interacting with hHSP90AA1, which is able to combine with the promoter of hNotch1 and inactivate its expression. Thus, our study revealed hPER3 as a critical positive regulator of hADSCs adipogenesis, which was different from the other types of cells, providing a critical role of it in treating obesity.
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