Using a mouse model of heart failure, a team of researchers recently discovered new mechanisms to help define how the spleen and heart coordinate physiological inflammation in cardiac repair.
Through the study published in the American Journal of Physiology-Heart and Circulation, the researchers at the University of South Florida (USF Health) has analyzed the interactions of the lipid mediator sphingosine-1-phosphate (S1P) in the spleen and heart during the transition from acute to chronic heart failure. Although we can survive without a spleen, evidence continues to mount that this abdominal organ plays a more valuable role in our physiological defenses than previously suspected.
“The spleen holds a whole army of immune cells and signaling molecules that can be rapidly mobilized to respond whenever a major injury like a heart attack or viral invasion occurs,” said Ganesh Halade, PhD, an associate professor of cardiovascular sciences at the University of South Florida Health (USF Health) Morsani College of Medicine.
Dr. Halade led a new preclinical study that analyzed the interactions of the lipid mediator sphingosine-1-phosphate (S1P) in the spleen and heart during the transition from acute to chronic heart failure.
The researchers discovered new cardiac repair mechanisms to help shed light on spleen-heart coordination of physiological inflammation in a mouse model of heart failure.