Small ubiquitin-like modifier (SUMO) proteins are a family of small proteins that modify the function of other proteins in cells. SUMOylation refers to posttranslational modifications by these proteins. Previous studies have revealed excessive SUMOylation can cause dysfunction in the endothelium lining of the heart and heart vessels, causing stroke, sudden cardiac death and other vascular complications. Increased SUMOylation impairs vascular function; however, the role of specific SUMOs in the regulation of vascular function is not completely understood.
Using multiple complementary approaches, Santosh Kumar, PhD, associate of Cardiovascular Medicine, and colleagues recently reported in American Journal of Physiology: Heart and Circular Physiology that hyper-SUMO2ylation impairs vascular endothelial function and increases vascular oxidative stress, whereas endogenous SUMO2 is essential for maintenance of normal physiological function of the vascular endothelium.
“The findings of the study may be useful for the future development of novel therapeutics for vascular diseases,” Kumar said.
The American Physiology Society recognized Kumar’s publication as APSselect with a Distinction in Scholarship for the month of December.