A Positive Feedback Loop Between CXCL16 and the Inflammatory Factors IL‐17A and TGF‐ <i>β</i> Promotes Large Artery Atherosclerosis by Activating the STAT3/NF‐ <i>κ</i> B Pathway

CXC chemokine ligand 16 (CXCL16) expression is often observed in studies related to atherosclerosis (AS). However, the process by which CXCL16 promotes AS is still unknown. CXCL16 has the potential to be a therapeutic target for atherosclerotic disease, and we studied whether CXCL16 expression in carotid atherosclerotic plaques is correlated with plaque stability. The results revealed that the expression level of CXCL16 in unstable plaques was greater than that in stable plaques (<i>p</i> < 0.05). In an in vitro model, CXCL16 promoted the expression of interleukin-17A (IL-17A) and transforming growth factor-<i>β</i> (TGF-<i>β</i>) and the release of STAT3/NF-<i>κ</i>B pathway-associated proteins by regulating the expression of IL-17A, TGF-<i>β</i>, and CXCL16. In conclusion, there is a positive feedback regulatory pathway between inflammatory factors and CXCL16 during the progression of carotid AS. Inflammatory factors and CXCL16 promote each other's expression and activate the STAT3/NF-<i>κ</i>B pathway to promote carotid AS. CXCL16 is highly expressed in carotid atherosclerotic plaques, affecting plaque stability and further leading to the development of AS-related diseases such as ischaemic stroke. Thus, we hypothesise that CXCL16 is a potential therapeutic target for treating AS and AS-related diseases.