Clonal Hematopoiesis of Indeterminate Potential (CHIP) is a condition characterized by the presence of genetic mutations in blood-forming cells, which can increase the risk of developing blood cancers and, importantly, cardiovascular diseases such as heart attacks and strokes. These mutations lead to an expansion of certain mutated blood cell clones, which in turn can promote chronic inflammation, a key contributor to cardiovascular disease.
Recent research has focused on understanding how CHIP mutations, particularly those involving genes like TET2 and DNMT3A, contribute to heightened inflammation and vascular damage. This has led to the hypothesis that targeting inflammation could be a potential therapeutic strategy to mitigate cardiovascular risks in individuals with CHIP.
In this elegant study by Zuriaga M. and coll. colchicine blunted atherosclerosis in the mouse model of TET2-mutant clonal hematopoiesis, in parallel with suppression of interleukin-1β overproduction in conditions of TET2 loss of function. While whole-exome sequencing data and clinical data from >450’000 patients showed that colchicine prescription jeopardized the associations between TET2 mutations and myocardial infarction.
Such important results quest for translation and future clinical trials that, when successful, would represent a significant breakthrough, transforming how cardiovascular risk is managed in individuals with CHIP, and potentially leading to more personalized treatment approaches.
Our mission: To reduce the burden of cardiovascular disease.