ArticleNature aging2025
Targeting the chromatin remodeler BAZ2B mitigates hepatic senescence and MASH fibrosis.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research trends of mitochondrial dysfunction in hepatic fibrosis: a bibliometric analysis.Frontiers in physiology · 2026Pooled it
- JMJD3-driven epigenetic reprogramming of p16Bone research · 2026Article
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Review
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- [Advances in research on metabolic associated fatty liver disease in 2025].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Targeting age-related LINE-1 activation alleviates cardiac aging.Nature aging · 2026Article
- Article
- Article
- Mapping the Intellectual Landscape: A 20-Year Bibliometric Analysis of Mechanisms in Metabolic Dysfunction-Associated Steatotic Liver Disease.Hepatic medicine : evidence and research · 2025Article
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
With increased age, the liver becomes more vulnerable to metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. Deciphering the complex interplay between aging, the emergence of senescent cells in the liver and MASH fibrosis is critical for developing treatments. Here we report an epigenetic mechanism that links liver aging to MASH fibrosis. We find that upregulation of the chromatin remodeler BAZ2B in a subpopulation of hepatocytes (HEPs) is linked to MASH pathology in patients. Genetic ablation or hepatocyte-specific knockdown of Baz2b in mice attenuates HEP senescence and MASH fibrosis by preserving peroxisome proliferator-activated receptor α (PPARα)-mediated lipid metabolism, which was impaired in both naturally aged and MASH mouse livers. Mechanistically, Baz2b downregulates the expression of genes related to the PPARα signaling pathway by directly binding their promoter regions and reducing chromatin accessibility. Thus, our study unravels the BAZ2B-PPARα-lipid metabolism axis as a link from liver aging to MASH fibrosis, suggesting that BAZ2B is a potential therapeutic target for HEP senescence and fibrosis.
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40389730What 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.