Inflammatory mechanisms and targeted drugs in heart failure

Heart failure (HF) is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Globally, the morbidity and mortality of HF are still on the rise, especially in elderly individuals, and the low 5-year survival rate of HF is a major social and health management problem. The pathogenesis of heart failure involves genetic factors and persistent cardiac inflammation. Genetic factors typically increase a patient's susceptibility to specific diseases. Notably, persistent cardiac inflammation is also a significant contributor to heart failure. Whether it is spontaneous aseptic inflammation of the heart or inflammation caused by infection, both can lead to excessive activation of the immune system, thereby triggering adverse cardiac remodeling. This review focuses on describing the inflammatory/immune activation mechanisms involved in heart failure and explores targeted drugs for inflammatory/immune activation. Additionally, we focused on the NLRP3 inflammasome (a cellular signaling protein complex), whose excessive activation produces large number of inflammatory factors, including IL-1β and IL-18, ultimately leading to persistent inflammation and excessive immune activation in the myocardium, which in turn triggers myocardial cell death and adverse remodeling. We have revealed the pathogenic role of NLRP3 in heart failure, providing a theoretical basis for further research into heart failure.