Banking on ATM as a new target in metabolic syndrome.
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.
Shoelson
Steven E
SE
Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA.
D000818:Animals; D051379:Mice; D064007:Ataxia Telangiectasia Mutated Proteins; D050197:Atherosclerosis / Q000188:drug therapy; D018797:Cell Cycle Proteins / Q000187:drug effects / Q000378:metabolism; D002738:Chloroquine / Q000627:therapeutic use; D004268:DNA-Binding Proteins / Q000187:drug effects / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects; D024821:Metabolic Syndrome / Q000188:drug therapy; D018345:Mice, Knockout / Q000235:genetics; D009154:Mutation; D010749:Phosphoprotein Phosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction; D025521:Tumor Suppressor Proteins / Q000187:drug effects / Q000378:metabolism; D054637:Dual-Specificity Phosphatases
D064007:Ataxia Telangiectasia Mutated Proteins; C576325:Atm protein, mouse; D018797:Cell Cycle Proteins; D002738:Chloroquine; D004268:DNA-Binding Proteins; D010749:Phosphoprotein Phosphatases; D017346:Protein Serine-Threonine Kinases; D025521:Tumor Suppressor Proteins; C522152:Dusp22 protein, mouse; D054637:Dual-Specificity Phosphatases