Metabolism and heart disease are intimately connected, with metabolic processes playing a critical role in the development and progression of cardiovascular conditions. The complex interplay between lipid metabolism, glucose metabolism, and mitochondrial function impacts the risk and pathogenesis of heart diseases. Lipid metabolism plays a central role in the development of atherosclerosis, the primary cause of coronary artery disease (CAD). Elevated levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides contribute to the formation of atherosclerotic plaques in arterial walls. Oxidized LDL particles can promote inflammation and the recruitment of immune cells, leading to the formation of foam cells, a hallmark of early atherosclerosis. High-density lipoprotein cholesterol (HDL-C), on the other hand, possesses anti-atherogenic properties by facilitating cholesterol efflux from macrophages in the arterial wall. Insulin resistance, a characteristic feature of type 2 diabetes, is also closely associated with an increased risk of heart disease. Chronic hyperglycaemia, resulting from impaired glucose metabolism, promotes oxidative stress and inflammation, contributing to endothelial dysfunction and blood vessel damage. Insulin resistance also has additional effects upon lipid metabolism, leading to dyslipidaemia and atherogenic lipoprotein profiles. Obesity and metabolic syndrome, characterized by a cluster of metabolic abnormalities (such as central obesity, hypertension, insulin resistance, and dyslipidaemia), also significantly increases the risk of heart disease. Adipose tissue, particularly visceral fat, secretes pro-inflammatory cytokines and adipokines, further contributing to systemic inflammation and ultimately to cardiovascular dysfunction. Mitochondrial dysfunction is also observed in heart failure, a prevalent condition associated with impaired cardiac function. The heart relies heavily on oxidative phosphorylation and efficient mitochondrial function for energy production. In heart failure, reduced mitochondrial ATP production and increased production of reactive oxygen species (ROS) can contribute to cardiac damage and dysfunction. During ischemic heart disease, such as myocardial infarction (heart attack), the heart experiences a temporary lack of oxygen and nutrients. To adapt to the ischemic conditions, cardiac myocytes undergo metabolic shifts, switching from aerobic to anaerobic metabolism, leading to the accumulation of lactate. Reperfusion following ischemia can also induce oxidative stress and mitochondrial dysfunction, contributing to reperfusion injury. Dyslipidaemia, characterized by abnormal lipid levels, is also a major risk factor for heart disease. Statins, a class of drugs that lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, are widely used to manage dyslipidaemia and therefore reduce cardiovascular risk. Finally, advancements in precision medicine have allowed personalized treatment approaches in heart disease. Genetic testing can identify individuals with familial hypercholesterolemia or other genetic predispositions to heart disease, allowing for targeted interventions and early detection. Lifestyle modifications, pharmacological interventions, and precision medicine approaches therefore offer promising avenues for reducing the burden of heart disease and enhancing patient outcomes. We offer a large product range of research reagents for studying heart disease, including IRS1 antibodies, RBP4 antibodies, Insulin antibodies, Leptin ELISA Kits, and Adiponectin ELISA Kits. Explore our full heart disease product range below and discover more, for less.