ArticleGenes2022
ASH2L Aggravates Fibrosis and Inflammation through HIPK2 in High Glucose-Induced Glomerular Mesangial Cells.
Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Chinese herbal medicine and its active compounds in attenuating renal injuryFrontiers in endocrinology · 2023Pooled it
- Beyond hyperglycemia: histone modification-mediated epigenetic dysregulation in diabetic retinopathy and nephropathy.Diabetology & metabolic syndrome · 2026Review
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- Functional role of Ash2l in oxLDL induced endothelial dysfunction and atherosclerosis.Cellular and molecular life sciences : CMLS · 2024Article
- The Sweet Side of HIPK2.Cancers · 2023Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and continues to be a threat to patients with diabetes. Dysfunction of glomerular mesangial cells (GMCs) is the main contributing factor to glomerulosclerosis, which is a pathological feature of DN. The epigenetic factor ASH2L has long been thought to be a transcriptional activator, but its function and involvement in diabetic nephropathy is still unclear. Here, we investigated the effect of ASH2L on the regulation of fibrosis and inflammation induced by high glucose in mouse mesangial cells (mMCs). We observed that ASH2L expression is increased in high glucose-induced mMCs, while loss of ASH2L alleviated fibrosis and inflammation. Furthermore, ASH2L-mediates H3K4me3 of the homeodomain-interacting protein kinase 2 (HIPK2) promoter region, which is a contributor to fibrosis in the kidneys and promotes its transcriptional expression. Similar to loss of ASH2L, silencing HIPK2 also inhibited fibrosis and inflammation. In addition, ASH2L and HIPK2 are upregulated in the kidneys of both streptozocin-induced and db/db mouse. In conclusion, we uncovered the crucial role of ASH2L in high glucose-induced fibrosis and inflammation, suggesting that ASH2L regulation may be an attractive approach to attenuate the progression of DN.
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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.