BMAL1 attenuates intervertebral disc degeneration by activating the SIRT1/PGC-1α pathway: evidence from vitro studies

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Publicado en:Scientific Reports (Nature Publisher Group) vol. 15, no. 1 (2025), p. 9651
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022 |a 2045-2322 
024 7 |a 10.1038/s41598-025-94029-7  |2 doi 
035 |a 3179585252 
045 2 |b d20250101  |b d20251231 
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245 1 |a BMAL1 attenuates intervertebral disc degeneration by activating the SIRT1/PGC-1α pathway: evidence from vitro studies 
260 |b Nature Publishing Group  |c 2025 
513 |a Journal Article 
520 3 |a To explore the potential effects and the corresponding mechanisms of brain and muscle arnt-like protein-1 (BMAL1) on the progression of intervertebral disc degeneration (IVDD) in vitro studies. The expression of BMAL1, SIRT1 and PINK1 were evaluated by the method of siRNA/pcDNA in the immortalized nucleus pulposus (NP) cells. The expression of SIRT1/PGC-1α pathway was assessed. The characteristics of NP cell, containing the activity and density, the level of apoptosis, inflammatory response, reactive oxygen species (ROS), senescence, and mitophagy were evaluated. The overexpression of BMAL1 was achieved with the pcDNA3.1, the expression of SIRT1 and PGC-1α were increased, the inflammatory response, the ROS, the level of apoptosis and senescence were decreased, however, the level of mitophagy, the activity and density of NP cell were enhanced. The BMAL1 inhibites the progression of IVDD by activating the SIRT1/PGC-1α pathway in the vitro studies. 
653 |a SIRT1 protein 
653 |a Reactive oxygen species 
653 |a Mitophagy 
653 |a Neurodegeneration 
653 |a PTEN-induced putative kinase 
653 |a Apoptosis 
653 |a Nucleus pulposus 
653 |a Senescence 
653 |a Intervertebral discs 
653 |a BMAL1 protein 
653 |a siRNA 
653 |a Inflammation 
653 |a Biosynthesis 
653 |a Metabolism 
653 |a Protein expression 
653 |a Oxidative stress 
653 |a Proteins 
653 |a Degenerative disc disease 
653 |a Back pain 
653 |a Aging 
653 |a Hospitals 
653 |a Cell growth 
653 |a Enzymes 
653 |a Environmental 
773 0 |t Scientific Reports (Nature Publisher Group)  |g vol. 15, no. 1 (2025), p. 9651 
786 0 |d ProQuest  |t Science Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3179585252/abstract/embedded/6A8EOT78XXH2IG52?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3179585252/fulltextPDF/embedded/6A8EOT78XXH2IG52?source=fedsrch