Lipolysis-stimulated lipoprotein receptor (LSR)

Lipolysis-stimulated lipoprotein receptor (LSR) is a membrane receptor primarily expressed in the liver and other tissues, where it mediates the hepatic uptake of triglyceride-rich remnant lipoproteins, particularly after lipolysis exposes binding sites for apolipoproteins B and E[1]. LSR also functions as a receptor on epithelial cells for certain bacterial binary toxins, such as Clostridium difficile transferase (CDT) and C. perfringens iota toxin, acting as a critical mediator of toxin internalization and cytotoxicity[2]. In addition, LSR has a structural role in organizing tricellular tight junctions, contributing to epithelial and blood–brain barrier integrity[3][4]. Genetic disruption of LSR leads to embryonic lethality in mice, and heterozygous inactivation causes increased plasma lipids and susceptibility to diet-induced atherosclerosis[1]. LSR is considered a novel therapeutic target for hyperlipidemia and possibly for infectious or barrier dysfunction-related diseases[1][2][3][4].

Other names

LSRAngulin-1ILDR3LISCH7Lipolysis-stimulated remnant receptorImmunoglobulin-like domain containing receptor 3LISCH proteinTricellulin recruitment factorLiver-specific bHLH-Zip transcription factor

For potential drugs: Inhibition or modulation of LSR would alter hepatic lipoprotein uptake and alter susceptibility to bacterial toxin uptake, or influence tight junction function