With the drug that inhibits HDAC9, we were able to decrease inflammation and remove cholesterol at the same time, said Mishra. This study suggests that specifically targeting HDAC9 without inhibiting other histone deacetylases will be helpful for atherosclerosis.
In a separate study, scientists found a potential explanation for why cells in lupus patients die at an increased rate and accumulate in tissues. This accumulation of cells is believed to trigger the inflammation that causes symptoms.
We have not previously understood why cells die at an increased rate, said Mishra. This new study suggests both a possible mechanism and treatment.
The study examined microRNAs, chains of ribonucleic acid that are involved in cell proliferation and cell death. The goal was to explore the possibility that aberrant expression of microRNAs is responsible for the abnormal cell death in lupus patients.
The scientists analyzed blood samples from five patients with lupus and seven healthy people of the same ages and sex at two points during a three-month period. A particular microRNA, miR-16, was consistently increased in lupus patients compared to the healthy participants. The scientists suspect that having too much miR-16 inhibits genes that control cell death and may also inhibit natural cell progression resulting in the accumulation in tissues.
Understanding this connection may lead to targeted treatments to decrease levels of miR-16, said Mishra.
|Contact: Karen Richardson|
Wake Forest University Baptist Medical Center