Our collaborative paper with the Laboratory of Laboratory Animal Science has just been published in PLOS ONE!

The first author is Dr. Hayato Sasaki from the Laboratory of Laboratory Animal Science, and the paper is titled:

"Protective function of the voltage-gated potassium channel Kv11.3 in a mouse model of cardiac ischemia/reperfusion injury"

🫀 The Study in a Nutshell

Voltage-gated potassium (Kv) channels are essential for controlling the electrical activity in excitable tissues like nerves and the heart. While Kv11.3 has been linked to bipolar disorder, its role in cardiac function had not been explored.

In this study, Kv11.3 knockout (KO) mice—mice genetically engineered to lack Kv11.3—underwent a cardiac ischemia/reperfusion (I/R) procedure, a model that mimics heart attacks. Surprisingly, compared to normal mice, the KO mice showed:

• Higher mortality and larger infarct (damaged) areas

• Abnormal heart rate variability

• Little to no shortening of the QT interval, unlike wild-type mice

When a Kv11.3 inhibitor (NS-1643) was administered to normal mice, the same adverse effects were observed, supporting the idea that Kv11.3 plays a protective role during cardiac stress. The protective effect appeared to be mediated not directly in the heart, but through neural pathways.

🔬 Our Contribution: Structural Insight from the Toxicology Lab

Our Toxicology Lab contributed by performing molecular docking and molecular dynamics simulations, providing 3D structural insight into Kv11.3’s function and helping to interpret the biological findings.

This marks our first collaborative paper with another lab on campus using our structural analysis approach—a major milestone for us!

🚀 Looking Ahead

Discoveries like this highlight how neural-cardiac molecular mechanisms can shape our understanding of both animal and human health.

We’ll continue using computational structural biology to accelerate veterinary research and uncover new mechanisms of disease and protection. Stay tuned for more!

DOI: https://doi.org/10.1371/journal.pone.0323428