News / New publications

Research

We work together for a better translational approach, from basic to clinical science

  • Read more

Core facilities

Our advanced core facilities offer excellent opportunities

  • Read more

Recruitment

We welcome the best research talents from Norway and the rest of the world

  • Read more

Archives IEMR

  • Publications
  • News archive
  • Visual profile

About IEMR

  • About
  • Funding
  • Collaborations
  • Staff

Contact IEMR

  • Contact
  • Group leaders
  • Leadership
  • Safety representative (VO)

New insights into reperfusion arrhythmias

CaMKII and reactive oxygen species contribute to early reperfusion arrhythmias, but oxidation of CaMKIIδ at methionines 281/282 is not a determining factor.

Marie Haugsten Hansen, Mani Sadredini, Almira Hasic, Mark E. Anderson, Ivar Sjaastad, Mathis Korseberg Stokke

A new paper from IEMR has given further support to the role of Ca2+/calmodulin-dependent kinase type II (CaMKII) and radical oxygen species (ROS) in reperfusion arrhythmias, but refuted a long-held hypothesis about this common clinical problem.

Reperfusion and return of blood flow to the ischemic area is key in the treatment of myocardial infarction, but can lead to further damage of the heart and arrhythmias. Arrhythmias are particularly common during the early reperfusion phase, and can complicate patient treatment, or in rare cases be fatal.

Early reperfusion arrhythmias result from abnormal calcium handling in cardiomyocytes. Evidence suggests that CaMKII and ROS are important for such perturbations. According to a key hypothesis, the two also interact by ROS-dependent activation of CaMKII.

To investigate this, Marie Synnøve Haugsten Hansen from the Stokke group, used hearts and isolated cells from normal mice, as well as mice with CaMKII resistant to oxidation (MMVV). Hearts and cells from both groups were exposed to protocols of ischemia and reperfusion. The results showed that CaMKII inhibition and ROS-scavenging reduced the incidence of arrhythmic events. However, mice with mutated CaMKII were not protected.

These results provide important insights into the mechanisms underlying reperfusion arrhythmias, and suggests potential strategies for future treatment.

 

DOI: https://doi.org/10.1016/j.yjmcc.2022.12.002

Marie Haugsten Hansen

Doctoral Research Fellow

  • View profile

Mathis Korseberg Stokke

Head of Department & Group Leader & Professor & Senior Consultant

  • View profile

Institute for Experimental Medical Research

Oslo University Hospital, Ullevål

PB 4956 Nydalen

NO-0424 Oslo

Norway

  • Research
  • Core facilities
  • Recruitment
  • Publications
  • News archive
  • Visual profile
  • About
  • Funding
  • Collaborations
  • Staff
  • Contact
  • Group leaders
  • Leadership
  • Safety representative (VO)