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January 2020 - Volume 75 - Issue 1

  • George W. Booz, PhD, FAHA
  • 0160-2446
  • 1533-4023
  • 12 issues per year
  • Cardiac & Cardiovascular Systems 69/136, Pharmacology & Pharmacy 151/267
  • 2.371

How do you mend a broken heart? Or at least an infarcted one. Increasing evidence indicates that stem cell therapy offers one way, but not through cardiac myocyte regeneration as originally envisioned. Rather, this approach likely provides a source of beneficial paracrine factors that help in the healing process. In a rapid communication that appears in the January issue, Ameri et al. focus their attention on one such factor, IL-15. They previously found that this peptide, a member of the four α-helix bundle family of cytokines, is present in a bone marrow-derived stem cell extract and protects isolated cardiac myocytes from hypoxia. The current study used a mouse model of myocardial infarction (MI) with IL-15 being administered by IP injection at 6 hour intervals, twice on the day of MI and 3 times on each of the following 2 days. The animals were monitored for 28 days. The investigators report that administration of IL-15 reduced cell death and scar size, increased vascularity, and improved left ventricular ejection fraction. Unresolved is what the molecular bases for these beneficial actions of IL-15 are. As pointed out by the authors, the actions of IL-15 are likely pleiotropic involving for instance modulating endoplasmic reticulum stress and glucose uptake, perhaps being mediated by STAT3 and ERK1/2 signaling. As they also note, immune-modularity effects of IL-15 may have come into play as well. As will be discussed in the February issue by Fouad Zouein and his team, the process of repair triggered by an MI involves the temporal recruitment of different immune cells. What effect IL-15 has on these cells in context awaits investigation.  

 

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