ArticleAging cell2020
The NSD2/WHSC1/MMSET methyltransferase prevents cellular senescence-associated epigenomic remodeling.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Histone demethylase KDM7A negatively regulates fibrotic macrophage polarization and lung fibrosis progression.Communications biology · 2026Article
- Comprehensive profiling of circRNAs reveals stimulus-specific networks and core regulators of cellular senescence.PloS one · 2026Article
- Epigenetic Factors in Pathogenesis of Retinoblastoma: DNA Methylation and Histone Acetylation.Current issues in molecular biology · 2025Review
- KDM4 Orchestrates Epigenomic Remodeling of Senescent Cells and Potentiates the Senescence-Associated Secretory Phenotype.Aging cell · 2025Article
- Article
- Exploring the uncharted role of cell senescence in rare diseases.Orphanet journal of rare diseases · 2025Review
- Histone Lactylation Antagonizes Senescence and Skeletal Muscle Aging by Modulating Aging-Related Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming.International journal of oral science · 2025Article
- SETD2 loss-of-function uniquely sensitizes cells to epigenetic targeting of NSD1-directed H3K36 methylation.Genome biology · 2025Article
- Epithelial NSD2 maintains FMO-mediated taurine biosynthesis to prevent intestinal barrier disruption.Clinical and translational medicine · 2024Article
- Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases.Human genomics · 2024Review
- Systematic perturbations of SETD2, NSD1, NSD2, NSD3, and ASH1L reveal their distinct contributions to H3K36 methylation.Genome biology · 2024Article
- Integrative analysis of the transcriptome and metabolome reveals the importance of hepatokine FGF21 in liver aging.Genes & diseases · 2024Article
- The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation.Cells · 2024Review
- Decreased NSD2 impairs stromal cell proliferation in human endometrium via reprogramming H3K36me2.Reproduction (Cambridge, England) · 2024Article
- Vutiglabridin Alleviates Cellular Senescence with Metabolic Regulation and Circadian Clock in Human Dermal Fibroblasts.Antioxidants (Basel, Switzerland) · 2024Article
- Loss of function inGenetics in medicine open · 2024Article
- The genomic response of human granulosa cells (KGN) to melatonin and specific agonists/antagonists to the melatonin receptors.Scientific reports · 2022Article
- 3-deazaadenosine (3DA) alleviates senescence to promote cellular fitness and cell therapy efficiency in mice.Nature aging · 2022Article
- METTL3 enhances NSD2 mRNA stability to reduce renal impairment and interstitial fibrosis in mice with diabetic nephropathy.BMC nephrology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent cells may possess the intrinsic programs of metabolic and epigenomic remodeling, but the molecular mechanism remains to be clarified. Using an RNAi-based screen of chromatin regulators, we found that knockdown of the NSD2/WHSC1/MMSET methyltransferase induced cellular senescence that augmented mitochondrial mass and oxidative phosphorylation in primary human fibroblasts. Transcriptome analysis showed that loss of NSD2 downregulated the expression of cell cycle-related genes in a retinoblastoma protein (RB)-mediated manner. Chromatin immunoprecipitation analyses further revealed that NSD2 was enriched at the gene bodies of actively transcribed genes, including cell cycle-related genes, and that loss of NSD2 decreased the levels of histone H3 lysine 36 trimethylation (H3K36me3) at these gene loci. Consistent with these findings, oncogene-induced or replicative senescent cells showed reduced NSD2 expression together with lower H3K36me3 levels at NSD2-enriched genes. In addition, we found that NSD2 gene was upregulated by serum stimulation and required for the induction of cell cycle-related genes. Indeed, in both mouse and human tissues and human cancer cell lines, the expression levels of NSD2 were positively correlated with those of cell cycle-related genes. These data reveal that NSD2 plays a pivotal role in epigenomic maintenance and cell cycle control to prevent cellular senescence.
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