ArticleMolecular biology reports2026
CBX3 aggravates nucleus pulposus cell apoptosis and extracellular matrix degradation in vitro via repressing SESN2-mediated mitophagy in an H3K9me3-dependent manner.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundMitophagy is crucial for maintaining mitochondrial quality and is implicated in intervertebral disc degeneration (IVDD). This study investigated the role and mechanism of Chromobox protein homolog 3 (CBX3) in IVDD, focusing on mitophagy regulation.
methodsAn in vitro IVDD model was established using interleukin (IL)-1β-treated nucleus pulposus cells (NPCs). RT-qPCR and western blot were applied to detect mRNA and protein expressions. Cell viability and apoptosis were examined with CCK-8 and flow cytometry, respectively. Immunofluorescence was conducted to measure colocalization of Mitotracker Red and LC3. Cellular ATP content was analyzed with the ATP detection kit. The molecular mechanism was explored using chromatin immunoprecipitation, peptide pull-down assay, and luciferase reporter assay.
resultsCBX3 was upregulated in IL-1β-stimulated NPCs. Its knockdown alleviated NPC apoptosis and extracellular matrix degradation, evidenced by reduced MMP3 and increased collagen II/aggrecan. Furthermore, CBX3 depletion restored PINK1/Parkin-mediated mitophagy, indicated by elevated PINK1/Parkin level, enhanced mitochondrial-LC3 colocalization and LC3II/I ratio, as well as decreased p62 protein level, and increased ATP levels. The mitophagy inhibitor Mdivi-1 reversed these protective effects of CBX3 knockdown. Mechanistically, CBX3 transcriptionally repressed sestrin2 (SESN2) in an H3K9me3-dependent manner. Silencing SESN2 abolished the benefits of CBX3 knockdown.
conclusionCBX3 repressed SESN2 transcription via an H3K9me3-dependent mechanism, leading to impaired PINK1/Parkin-mediated mitophagy, which in turn promoted NPC apoptosis and matrix degradation. This study identified a promising therapeutic target for IVDD.
Indexed as
Identifiers
42776360What OpenQuestion holds
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.