Reverse cholesterol transport (RCT) is a process that promotes the efflux of cholesterol from the cells and transports it to the liver for metabolism. Its dysfunction plays a key role in the development of atherosclerosis (As). Chronic metabolic inflammatory diseases including diabetes, obesity promote the progress of As, in which pro-inflammatory cytokines and adipokines are important regulatory mechanisms for the regulation of RCT in vivo. The research papers and review collected in this issue studied the effect of nuclear factor κB (NF-κB), glycosylation end products Nε-carboxymethyllysine, adipokines Visfatin, etc. on the cholesterol efflux and the expression of key proteins such as adenosine triphosphate binding cassette transporter A1, Sortilin, and acyl-coenzyme A:cholesterol acyltransferase (ACAT) in RCT, which would clarify the molecular mechanism of chronic metabolic inflammatory diseases regulating RCT and cardiovascular disease development from different perspectives.