A new research from Wake Forest University Baptist Medical Center has provided clues about the causes of lupus and has suggested specific new targeted treatment strategies.
The study was presented at the American College of Rheumatology in Boston.
During the study, researchers looked at premature atherosclerosis in lupus patients as well as accelerated cell death that seems to be behind many of the disease’s symptoms.
In one study, Nilamadham Mishra, M.D., from Wake Forest University Baptist Medical Center and colleagues looked at the potential mechanisms of premature atherosclerosis, which is one of the leading causes of death and disability in lupus patients. They found that even when they take drugs to lower their cholesterol, lupus patients still develop fatty buildups in their vessels, which can lead to heart attack and stroke.
Previous studies by Mishra found that a new class of drugs being developed (histone deacetylase inhibitors) were effective at preventing atherosclerosis in mice prone to develop the disease.
In the current study, Mishra and colleagues explored whether it is a specific histone deacetylase, number 9 (HDAC9) that causes the problem.
Histones are considered the master regulators in gene expression, and Mishra is the first to establish a link between abnormal histone codes and the complications of lupus in a mouse model of lupus.
The current study has revealed that in atherosclerosis-prone mice, there is more HDAC9 than usual in the macrophages, which are cells within the artery walls that collect cholesterol and can lead to atherosclerosis.