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June 2019 - Volume 73 - Issue 6

  • George W. Booz, PhD, FAHA
  • 0160-2446
  • 1533-4023
  • 12 issues per year
  • Cardiac & Cardiovascular Systems 66/125, Pharmacology & Pharmacy 155/254
  • 2.227

Ischemic injury to the heart triggers sterile inflammation that activates the NLRP3 inflammasome.  Activation of this intracellular macromolecular sensor of intracellular danger and tissue injury amplifies the inflammatory response causing further damage to the heart. In the July issue, an original study titled Pharmacologic inhibition of the NLRP3 inflammasome preserves cardiac function after ischemic and non-ischemic cardiac injury in the mouse, by Marchetti et al. presents evidence that a novel NLRP3 inflammasome inhibitor, 16673-34-0 limits cell death and left ventricular systolic dysfunction following injury to the mouse heart from ischemia, ischemia-reperfusion, or doxorubicin. 16673-34-0 is an intermediate in the synthesis of glyburide and was previously shown to prevent formation of the NLRP3 inflammasome in vitro and limit infarct size in the mouse heart. The results of the present study showing beneficial effects of 16673-34-0 in preserving cardiac function in 3 distinct models of cardiac injury lend further support to the translational potential of targeting the NLRP3 inflammasome to protect the heart. 

-George Booz, Editor-In-Chief

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