Scientists at the University of Texas Medical Branch at Galveston say they have discovered one of the pathogenic components of diabetes in the heart. Their paper (“Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C signaling) is published in the Journal of Biological Chemistry.
While both heart disease and diabetes are widely studied, how diabetic cardiomyopathy develops is not well understood, other than that it seemed to be linked to protein kinase C (PKC), a family of enzymes that controls the functions of other proteins by using phosphates to turn them on and off.
Researchers at UTMB, led by assistant professor of biochemistry Muge Kuyumcu-Martinez, Ph.D., studied the effects of PKC signals in the hearts of diabetic mice.
“We wanted to test whether PKC activation in diabetic hearts induces alternative splicing abnormalities,” wrote the investigators. “Using RNA sequencing we identified a set of 22 alternative splicing events that undergo a developmental switch in splicing and confirmed that splicing reverts to an embryonic pattern in adult diabetic hearts.…These findings provide a basis for PKC-mediated cardiac pathogenesis under diabetic conditions.”
“We now know that the leading cause of diabetic cardiomyopathy can be attributed to PKC activation and its downstream effects on gene expression,” said Dr. Kuyumcu-Martinez. “Knowing how cardiomyopathy manifests, further research can use these results to concentrate on the prevention and treatment of heart failure in diabetics.”