scholarly journals Combination of Heart-Type Fatty Acid Binding Protein and Brain Natriuretic Peptide Can Reliably Risk Stratify Patients Hospitalized for Chronic Heart Failure

2005 ◽  
Vol 69 (8) ◽  
pp. 922-927 ◽  
Author(s):  
Takeshi Niizeki ◽  
Yasuchika Takeishi ◽  
Takanori Arimoto ◽  
Tatsuya Takahashi ◽  
Hidenobu Okuyama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Fatty Acid ◽  
Chronic Heart Failure ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

scholarly journals Role of the fatty acid-binding protein 4 in heart failure and cardiovascular disease

2017 ◽  
Vol 233 (3) ◽  
pp. R173-R184 ◽  
Author(s):  
Ricardo Rodríguez-Calvo ◽  
Josefa Girona ◽  
Josep M Alegret ◽  
Alba Bosquet ◽  
Daiana Ibarretxe ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Left Ventricular ◽  
Aetiological Factor ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

Obesity and ectopic fat accumulation in non-adipose tissues are major contributors to heart failure (HF) and cardiovascular disease (CVD). Adipocytes act as endocrine organs by releasing a large number of bioactive molecules into the bloodstream, which participate in a communication network between white adipose tissue and other organs, including the heart. Among these molecules, fatty acid-binding protein 4 (FABP4) has recently been shown to increase cardiometabolic risk. Both clinical and experimental evidence have identified FABP4 as a relevant player in atherosclerosis and coronary artery disease, and it has been directly related to cardiac alterations such as left ventricular hypertrophy (LVH) and both systolic and diastolic cardiac dysfunction. The available interventional studies preclude the establishment of a direct causal role of this molecule in CVD and HF and propose FABP4 as a biomarker rather than as an aetiological factor. However, several experimental reports have suggested that FABP4 may act as a direct contributor to cardiac metabolism and physiopathology, and the pharmacological targeting of FABP4 may restore some of the metabolic alterations that are conducive to CVD and HF. Here, we review the current knowledge regarding FABP4 in the context of HF and CVD as well as the molecular basis by which this protein participates in the regulation of cardiac function.

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