ArticleAging cell2014
Deleted in Breast Cancer 1 regulates cellular senescence during obesity.
Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- The DBC1-HIF-1α-PPAR-γ axis regulates Treg cell differentiation to promote myocardial fibrosis in experimental diabetic cardiomyopathy through the paracrine secretion of Areg.Frontiers in endocrinology · 2026Article
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- The Influence of Body Mass Index on Biomarkers of Cellular Senescence in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Adipocyte-specific deletion of Dbc1 does not recapitulate healthy obesity phenotype but suggests regulation of inflammation signaling.PloS one · 2025Article
- Targeting Cell Senescence and Senolytics: Novel Interventions for Age-Related Endocrine Dysfunction.Endocrine reviews · 2024Review
- Review
- Article
- Targeting cellular senescence in metabolic disease.Molecular metabolism · 2022Review
- Review
- Senescent cells in human adipose tissue: A cross-sectional study.Obesity (Silver Spring, Md.) · 2021Article
- The role of cellular senescence in ageing and endocrine disease.Nature reviews. Endocrinology · 2020Review
- The protein Deleted in Breast Cancer-1 (DBC1) regulates vascular response and formation of aortic dissection during Angiotensin II infusion.Scientific reports · 2020Article
- Human Obesity Induces Dysfunction and Early Senescence in Adipose Tissue-Derived Mesenchymal Stromal/Stem Cells.Frontiers in cell and developmental biology · 2020Article
- A novel form of Deleted in breast cancer 1 (DBC1) lacking the N-terminal domain does not bind SIRT1 and is dynamically regulated in vivo.Scientific reports · 2019Article
- Loss of DBC1 (CCAR2) affects TNFα-induced lipolysis andJournal of molecular endocrinology · 2018Article
- Nrf2 Deficiency Exacerbates Obesity-Induced Oxidative Stress, Neurovascular Dysfunction, Blood-Brain Barrier Disruption, Neuroinflammation, Amyloidogenic Gene Expression, and Cognitive Decline in Mice, Mimicking the Aging Phenotype.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
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- Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic obesity leads to inflammation, tissue dysfunction, and cellular senescence. It was proposed that cellular senescence during obesity and aging drives inflammation and dysfunction. Consistent with this, clearance of senescent cells increases healthspan in progeroid mice. Here, we show that the protein Deleted in Breast Cancer-1 (DBC1) regulates cellular senescence during obesity. Deletion of DBC1 protects preadipocytes against cellular senescence and senescence-driven inflammation. Furthermore, we show protection against cellular senescence in DBC1 KO mice during obesity. Finally, we found that DBC1 participates in the onset of cellular senescence in response to cell damage by mechanism that involves binding and inhibition of HDAC3. We propose that by regulating HDAC3 activity during cellular damage, DBC1 participates in the fate decision that leads to the establishment of cellular senescence and consequently to inflammation and tissue dysfunction during obesity.
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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.