Scientists have shown that aspirin can directly affect genes in blood platelets and this results in its blood thinning benefits.
Deepak Voora, MD, assistant professor in Duke’s Center for Applied Genomics & Precision Medicine led a team, which analysed the direct genome effects of the cheap pain-killer and identified the new pathway. Apparently, aspirin affects the function of RUNX1, a regulatory protein.
It was already known that aspirin affected the function of COX1, which is the producer of inflammation, causing it to calm down. COX1 is also known to affect blood clotting.
Chris Woollams said, “This work should silencing the growing band of people who have been publicly pouring scorn on claims of benefits for aspirin in cardiovascular disease. Here the scientists found a new mechanism of action by directly studying the affects on the genome”.
Voora’s team had previously shown that a pair of genes were modified by exposure to aspirin. In this study they showed how aspirin worked on them. Aspirin binds to an intermediary – a transcription factor which regulates the two genes. RUNX1 expression was also linked with reduced cardiovascular incident, and better long-term outcomes.
