Heart failure (HF) is a rapidly growing public health issue, with an estimated prevalence of 64 million people globally. The prevalence of HF continues to increase due to population aging and the increasing prevalence of obesity, diabetes, and hypertension. Despite therapeutic progress, HF remains associated with high mortality, significant morbidity, poor quality of life and functional capacity, and a substantial health burden. The five-year mortality rate for HF patients is approximately 50% to 60% and is even higher among patients requiring hospitalisation.
While there are evidence-based therapies for HF with reduced ejection fraction (HFrEF), effective therapies for HF with preserved ejection fraction (HFpEF) remain limited, reflecting an incomplete understanding of its multifactorial pathophysiology. The underlying pathophysiology of HF, particularly HFpEF, is complex and has not been fully elucidated. Our research, employing both preclinical and clinical approaches, has demonstrated the pivotal role of hypertension, diabetes, and obesity as drivers of inflammation, myocardial fibrosis, and metabolic disorders.
This program aims to address critical knowledge gaps through integrated metabolomic and proteomic analyses to elucidate mechanisms underlying HF onset and progression. We will identify the molecular drivers of inflammation, fibrosis, and metabolic dysfunction that distinguish HFpEF from HFrEF. These data will establish a mechanistic framework for target discovery and therapeutic development. In parallel, we will define the cellular biology of cardiac fibrosis and leverage our expertise in drug development to advance first-in-class therapeutic candidates capable of preventing or reversing HF progression.