Eola1, also known as endothelial-overexpressed lipopolysaccharide-associated factor 1, is a gene that plays a role in inflammatory regulation [1,2,3,4]. It is associated with the regulation of proteins involved in the inflammatory response, such as interleukin-6 (IL-6) and vascular cell adhesion molecule-1 (VCAM-1), and may also prevent apoptosis in endothelial cells. Eola1 seems to function through its association with metallothionein 2A (MT2A) [1,3]. Understanding Eola1's function is crucial as endothelial cell injury or dysfunction, at least in part mediated by lipopolysaccharide (LPS), is related to various pathological conditions [3].

In ECV304 cells, Eola1 knockdown leads to a significant enhancement of LPS-induced VCAM-1 production, while its overexpression reduces such production. MT2A knockdown also reduces LPS-induced VCAM-1 production, indicating a negative regulatory role of Eola1 on LPS-induced VCAM-1 expression via its association with MT2A [1]. In human umbilical vein endothelial cells (HUVEC), deletion of Eola1 promotes IL-6 production and apoptosis induced by LPS treatment, suggesting that Eola1 may act as a negative regulator for LPS response by regulating MT2A [3]. In patients with diabetic foot ulcer, the expression of Eola1 in chronic wound group is significantly lower than that in acute wound group, and the expression of inflammatory factors NF-κB and IL-6 is increased, indicating a possible link between reduced Eola1 expression and uncontrolled inflammation [4].

In conclusion, Eola1 is an important intracellular protein involved in the negative regulation of the inflammatory response, especially in endothelial cells. Its association with MT2A is crucial in this process. Studies on Eola1's function, including those using knockdown models, have provided insights into its role in inflammation-related diseases such as endothelial cell-mediated disorders and diabetic foot ulcers.