Adipokines and Their Role in Heart Failure: A Literature Review

Obesity is a major risk factor for heart failure (HF). The relationship between adipokines and HF has been implicated in many previous studies and reviews. However, this review article summarizes the basic role of major adipokines, such as apelin, adiponectin, chemerin, resistin, retinol-binding protein 4 (RBP4), vaspin, visfatin, plasminogen activator inhibitor-1, monocyte chemotactic protein-1, nesfatin-1, progranulin, leptin, omentin-1, lipocalin-2, and follistatin-like 1 (FSTL1), in the pathogenesis of HF. Apelin is reduced in patients with HF and upregulated following favorable left ventricular (LV) remodeling. Higher levels of adiponectin have been found in patients with HF compared to in control patients. Also, high plasma chemerin levels are linked to a higher risk of HF. Serum resistin is related to the severity of HF and associated with a high risk for adverse cardiac events. Evidence indicates that RBP4 can contribute to inflammation and damage heart muscle cells, potentially leading to HF. Vaspin might stop the progression of cardiac degeneration, fibrosis, and HF according to experiments on rats with experimental isoproterenol-induced chronic HF. The serum concentrations of visfatin are significantly lower in patients with systolic HF. Leptin levels were found to be correlated with low LV mass and myocardial stiffness, both of which are significant risk factors for the development of HF with preserved ejection fraction (HFpEF). Measuring serum omentin-1 levels appears to be a novel prognostic indicator for risk stratification in HF patients. Increased expression of neutrophil gelatinase–associated lipocalin in both systemic circulation and myocardium in clinical and experimental HF suggests that innate immune responses may contribute to the development of HF. FSTL1 was elevated in patients with HF with reduced ejection fraction and associated with an increase in the size of the left ventricle of the heart. However, other adipokines, such as plasminogen activator inhibitor-1, monocyte chemotactic protein-1, nesfatin-1, and progranulin, have not yet been studied for HF.