Studies in blood vessel biology have resulted in new treatments for pulmonary hypertension and safer therapeutic strategies targeting angiotensin. This work is paving the way for improved treatments of accelerated atherosclerosis associated with autoimmune disorders such as rheumatoid arthritis.
The walls of our arteries are not passive structures. They respond, adapt and — when things go wrong — remodel in ways that can have serious consequences for health. Understanding exactly what drives those changes has been a central focus of Baker Institute research for decades.
Three interconnected areas of discovery stand out.
In the field of endothelin research, Baker Institute scientists were the first to demonstrate that endothelin-1 — a compound that constricts blood vessels — also stimulates the proliferation of the smooth muscle cells that make up artery walls. This finding ultimately led to the development of endothelin-1 antagonist drugs now used clinically in the treatment of pulmonary arterial hypertension, a serious and potentially fatal condition.
In studying angiotensin II, Baker Institute researchers made a pivotal discovery: this compound is essential for normal development of the blood vessels themselves. The finding led to worldwide recommendations that angiotensin-blocking drugs should be avoided during pregnancy — a direct translation of laboratory science into clinical safety practice.
Perhaps most unexpectedly, atherosclerosis research at the Baker Institute revealed that specific types of white blood cells — B cells — play a major role in the development of arterial plaque. This concept-changing discovery has opened new avenues for preventing the accelerated atherosclerosis seen in people with autoimmune diseases such as rheumatoid arthritis, where B cell-targeted therapies are already used to treat active disease.
