ArticleCell communication and signaling : CCS2026
Down-regulation of EHMT2 through irisin-mediated epigenetic modification promotes osteogenesis via promoting DLX3 transcription.
Article in Cell communication and signaling : CCS, 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
9 authors.
Funding
Abstract
backgroundIrisin, a cleavage peptide by fibronectin type III domain-containing protein 5 (FNDC5), has been recognized as a promotor of osteogenesis to alleviate osteoporosis (OP). However, the detailed regulatory mechanism of osteogenesis remains unclear. This study uncovered the mechanisms underlying bone formation.
methodsOsteogenic activity was evaluated by ALP and ARS staining. Expression of target molecules and osteogenic-related factors was assessed by RT-qPCR, Western blotting, and immunohistochemical staining. The binding of euchromatic histone lysine methyltransferase 2 (EHMT2) to distal-less homeobox 3 (DLX3) promoter was validated by ChIP and luciferase reporter assays. Protein interaction, ubiquitination, and small ubiquitin-like modifier (SUMO) modification were determined by Co-IP or Ni2+-NTA pull-down assay. In vivo bone formation was evaluated in a mouse model. Histological analysis was performed by HE and Masson staining.
resultsEHMT2 expression was decreased, while DLX3 expression was increased during osteogenic differentiation in vitro. Down-regulation of EHMT2 facilitated osteogenesis via enhancing DLX3 transcription and expression with assistance of H3K9me2. Moreover, EHMT2 was down-regulated by S-phase kinase-associated protein 2 (SKP2)-mediated ubiquitination, whereas protein inhibitor of activated STAT 4 (PIAS4)-mediated SUMOylation exerted an opposite role. Finally, irisin down-regulated EHMT2 via repressing SUMOylation and promoting ubiquitination of EHMT2, thus contributing to bone formation.
conclusionEpigenetic modification-mediated down-regulation of EHMT2 by irisin leads to transcriptional activation of DLX3, thus promoting bone formation.
Indexed as
Identifiers
What 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.