Clonal Hematopoiesis At The Crossroads Of Inflammaging And Cardiovascular Disease: Mechanistic Insights And Translational Horizons
As we age, our bodies undergo many changes, some of which can increase our risk for various diseases. One such change involves our blood-forming stem cells, which can acquire specific genetic mutations over time. This phenomenon is known as clonal hematopoiesis of indeterminate potential, or CHIP. While it might sound complex, think of it as certain blood stem cells gaining a slight advantage and multiplying more than others, leading to a “clone” of these slightly altered cells in the blood.
Recent research has highlighted that CHIP is not just an interesting biological observation; it’s a crucial, independent risk factor for serious cardiovascular diseases like heart attacks, strokes, and coronary artery disease. The key to this connection lies in inflammation. The mutated blood cells, particularly those that develop into certain immune cells (myeloid cells), become more prone to releasing inflammatory signals, such as IL-1β and IL-6. This creates a chronic, low-grade inflammatory environment throughout the body, a process sometimes called “inflammaging.”
This persistent inflammation contributes to the instability of plaques in our arteries, increasing the risk of blood clots and accelerating the aging of our blood vessels. Essentially, CHIP acts as a bridge connecting the natural process of aging with inflammation and the development of cardiovascular disease.
While routine screening for CHIP isn’t currently recommended for everyone, understanding its role opens doors for new strategies. For individuals at high risk, identifying CHIP could lead to more personalized preventive measures. Further research is ongoing to explore how integrating CHIP status into risk assessments could lead to more precise ways to prevent and manage age-related heart conditions.
Source: link to paper