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<p>Failure to reperfuse the coronary microvasculature (“no-reflow”) affects up to 50% of patients after unblocking a coronary artery that was causing ischaemia and acute myocardial infarction. This “no-reflow” is associated with reduced left ventricular ejection fraction, increased infarct size and death. We show that the incretin hormone&#xa0;GLP-1 (glucagon-like peptide 1) can be used to protect the heart after ischaemia by activating ATP-sensitive K<sup>+</sup> channels on pericytes that constrict coronary capillaries. Coronary capillary dilation can be activated pharmacologically or by vagally-mediated GLP-1 release from the gut evoked by skeletal muscle ischaemia, and is abolished by block or genetic deletion of pericyte K<sub>ATP</sub> channels. These results define a brain-gut-heart pathway mediating cardioprotection and suggest pharmacological therapies to reduce ischaemia-induced coronary no-reflow and improve post-infarct recovery.</p>

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GLP-1 activates KATP channels in coronary pericytes as the effector of brain-gut-heart signalling mediating cardioprotection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月14日

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  • Svetlana Mastitskaya,
  • Felipe Santos Simões de Freitas,
  • Lowri E. Evans,
  • David Attwell

摘要

Failure to reperfuse the coronary microvasculature (“no-reflow”) affects up to 50% of patients after unblocking a coronary artery that was causing ischaemia and acute myocardial infarction. This “no-reflow” is associated with reduced left ventricular ejection fraction, increased infarct size and death. We show that the incretin hormone GLP-1 (glucagon-like peptide 1) can be used to protect the heart after ischaemia by activating ATP-sensitive K+ channels on pericytes that constrict coronary capillaries. Coronary capillary dilation can be activated pharmacologically or by vagally-mediated GLP-1 release from the gut evoked by skeletal muscle ischaemia, and is abolished by block or genetic deletion of pericyte KATP channels. These results define a brain-gut-heart pathway mediating cardioprotection and suggest pharmacological therapies to reduce ischaemia-induced coronary no-reflow and improve post-infarct recovery.