Redistributing BRD4 in inflammation
New clues to how inflammation leads to atherosclerosis from a group at Harvard Medical School point to a pivotal role for chromosomal redistribution of BRD4-a BET bromodomain protein involved in chromatin remodeling.1 The data provide insight to the mechanism of BRD4 inhibitors in the clinic for atherosclerosis, but whether the compounds offer advantages over the standard of care still needs to be tested.
"This work provides a different lens for identifying novel players that are involved in endothelial inflammation and atherosclerosis and new insights into how such responses are regulated at the epigenetic level," said Jorge Plutzky, one of the study's senior investigators. Plutzky is director of the preventive cardiology at Brigham and Women's Hospital and a member of the faculty at Harvard Medical School.
The team was co-led by James Bradner, an investigator in the Department of Medical Oncology at the Dana-Farber Cancer Institute and founder of Tensha Therapeutics Inc., which has the BET bromodomain inhibitor TEN-010 in Phase I testing for solid tumors. Bradner also is cofounder of Syros Pharmaceuticals Inc., a faculty member at Harvard