Depletion of ASK1 blunts stress-induced senescence in adipocytes

Stephan Wueest, Fabrizio C. Lucchini, Yulia Haim, Assaf Rudich, Daniel Konrad

Research output: Contribution to journalArticlepeer-review


Increasing energy expenditure via induction of browning in white adipose tissue has emerged as a potential strategy to treat obesity and associated metabolic complications. We previously reported that ASK1 inhibition in adipocytes protected from high-fat diet (HFD) or lipopolysaccharide (LPS)-mediated downregulation of UCP1 both in vitro and in vivo. Conversely, adipocyte-specific ASK1 overexpression attenuated cold-induction of UCP-1 in inguinal fat. Herein, we provide evidence that both TNFα-mediated and HFD-induced activation of p38 MAPK in white adipocytes are ASK1-dependent. Moreover, expression of senescence markers was reduced in HFD-fed adipocyte-specific ASK1 knockout mice. Similarly, LPS-induced upregulation of senescence markers was blunted in ASK1-depleted adipocytes. Thus, our study identifies a previously unknown role for ASK1 in the induction of stress-induced senescence.

Original languageAmerican English
Pages (from-to)535-541
Number of pages7
Issue number1
StatePublished - 1 Jan 2020


  • Obesity
  • adipose tissue
  • browning
  • diabetes
  • lipopolysaccharide
  • p38 MAPK
  • subcutaneous

All Science Journal Classification (ASJC) codes

  • Cell Biology
  • Histology


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