Banking on ATM as a new target in metabolic syndrome

Cell Metab. 2006 Nov;4(5):337-8. doi: 10.1016/j.cmet.2006.10.009.


In this issue of Cell Metabolism, Semenkovich and his colleagues show that ATM, a protein well known for its roles in the cellular response to DNA breaks, may also be linked to metabolic and cardiovascular diseases (Schneider et al., 2006). ATM seemingly does this by inhibiting JNK, a stress kinase involved in inflammation with related effects in insulin resistance and atherosclerosis. In an interesting twist, the authors show that chloroquine, an antimalarial drug, also activates ATM, which inhibits JNK, and improves insulin sensitivity and cardiovascular effects. These findings provide potential new insights into the pathogenesis and treatment of metabolic syndrome.

Publication types

  • Review
  • Comment

MeSH terms

  • Animals
  • Ataxia Telangiectasia Mutated Proteins
  • Atherosclerosis / drug therapy
  • Cell Cycle Proteins / drug effects*
  • Cell Cycle Proteins / metabolism
  • Chloroquine / therapeutic use*
  • DNA-Binding Proteins / drug effects*
  • DNA-Binding Proteins / metabolism
  • Macrophages / drug effects
  • Metabolic Syndrome / drug therapy*
  • Mice
  • Mice, Knockout / genetics*
  • Mutation
  • Phosphoprotein Phosphatases / antagonists & inhibitors
  • Phosphoprotein Phosphatases / metabolism
  • Protein-Serine-Threonine Kinases / drug effects*
  • Protein-Serine-Threonine Kinases / metabolism
  • Signal Transduction
  • Tumor Suppressor Proteins / drug effects*
  • Tumor Suppressor Proteins / metabolism


  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Tumor Suppressor Proteins
  • Chloroquine
  • Ataxia Telangiectasia Mutated Proteins
  • Atm protein, mouse
  • Protein-Serine-Threonine Kinases
  • JKAP protein, mouse
  • Phosphoprotein Phosphatases