Deleted in Breast cancer 1 regulates cellular senescence during obesity

Carlos Escande, Veronica Nin, Tamar Pirtskhalava, Claudia C. Chini, Maria Thereza Barbosa, Angela Mathison, Raul Urrutia, Tamar Tchkonia, James L. Kirkland, Eduardo N. Chini

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)951-953
Number of pages3
JournalAging Cell
Issue number5
StatePublished - Oct 1 2014


  • Aging
  • Hdacs
  • Mice
  • Obesity
  • Senescence
  • Signaling
  • Sir2

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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