AEBP1 or ACLP, which is the key factor in inflammation and fibrosis?

Abstract

Adipocyte enhancer-binding protein 1 (AEBP1) and Aortic carboxypeptidase-like protein (ACLP) are two protein isoforms produced by the AEBP1 gene. AEBP1, originally discovered in preadipocytes, functions as a transcriptional repressor and is involved in promoting inflammation, proliferation, and migration through various signaling pathways. ACLP is an extracellular matrix protein linked to Ehlers-Danlos syndrome, a genetic disorder characterized by defective connective tissue development. Structurally, AEBP1 and ACLP share many similarities, and both participate in critical physiological or pathological processes, such as cancer and fibrosis, by influencing pathways like NK-κB, WNT, and TGF-β. In recent years, research on AEBP1 and ACLP has expanded to include major organs such as the brain, kidneys, and lungs, with a particular focus on the cardiovascular system, where they show potential as novel drug targets. However, most studies do not clearly distinguish between AEBP1 and ACLP. For instance, AEBP1 is implicated in myocardial fibrosis in hypertrophic cardiomyopathy models, whereas ACLP is associated with fibrosis in other organs. Additionally, literature on the relationship between AEBP1 and fibrosis is often contradictory. Clarifying the distinct roles of AEBP1 and ACLP and their different functions in various cell types would greatly benefit further research.

Current research suggests that the AEBP1 gene encodes two proteins, AEBP1 and ACLP, which have been reported to exhibit distinct functions in different studies. However, many studies do not differentiate between these two proteins, potentially leading to misconceptions. Therefore, we have conducted a comprehensive review of the existing literature to elucidate the functions of the AEBP1 gene and its encoded proteins in detail.