The discovery of a link between excess production of TNF and the development of heart valve disease may help identify patients most likely to respond to anti-TNF therapy, Australian researchers say.
The findings also suggest anti-TNF drugs may have a role to play in treating heart valve diseases such as rheumatic heart disease, according to the research team led by molecular biologist Dr Philippe Bouillet from the Walter and Eliza Hall Institute in Melbourne.
“To our knowledge, this is the first animal model showing both polyarthritis and heart disease as a direct result of TNF deregulation,” the researchers wrote.
“We could essentially develop agents that put a spanner in the works, stopping the factory production of TNF,” said Dr Bouillet.
The results showed that 30 years after TNF was first cloned key pathways governing its regulation were still being discovered.
“Once fully elucidated, we shall be able to screen for alterations in these regulatory mechanisms and hence aid in the identification of patients most likely to respond to anti-TNF therapies,” they wrote.
“We anticipate that our BPSM1 mice will be very valuable for the preclinical evaluation of therapies relevant to heart valve disease and rheumatoid arthritis,” they added.