Leptin–VEGF crosstalk in excess body mass and related disorders: A systematic review

Abstract

SummaryBy 2030, it is expected that a billion people will have suffer from obesity. Adipose tissue synthesizes leptin, an adipokine that affects cardiovascular risk. Leptin intensifies the synthesis of vascular endothelial growth factor (VEGF). Our study reviews recent reports on leptin–VEGF crosstalk in obesity and related disorders. PubMed, Web of Science, Scopus, and Google Scholar were searched. One hundred and one articles involving human, animal, and in vitro research were included. In vitro studies show the crucial role of interaction between endothelial cells and adipocytes and hypoxia as a factor that intensifies leptin's effects on VEGF. Leptin–VEGF crosstalk promotes the progression of cancer. The animal research reveal that a high‐fat diet enhances leptin and VEGF crosstalk. Genetic and epigenetic mechanisms and procreator‐offspring programming may be involved in leptin–VEGF crosstalk. Some female‐specific characteristics of leptin–VEGF relation in obesity were observed. The human studies have shown that increased leptin and VEGF synthesis and leptin–VEGF crosstalk are factors linking obesity with elevated cardiovascular risk. The studies of the last 10 years documented a range of significant aspects of leptin–VEGF crosstalk specific for obesity and related disorders, shedding new light on the link between obesity and increased cardiovascular risk.