Corrigendum to: Sortilin as a Culprit in the Atherosclerosis Plaque Progression: Evidence from Clinical and Experimental Studies.

It has come to our attention that in the published version of this article [1], reference [86] was cited erroneously; this has now been corrected. The original article can be found online at: https://www.eurekaselect.com/article/145963 Details of the correction are as follows: Original: These contradictory reports regarding the sortilin function in lipid metabolism may result from variations in employed animal models or lipid metabolic milieu. Once the intracellular level of apoB-100 is elevated, sortilin may primarily act as "the degrader," whereby sortilin can target VLDL to the lysosomal degradation and thus reduce the secretion of VLDL particles [28]. Oppositely, in situations of reduced expression of apoB-100, like in the DKO mouse model, sortilin can also exhibit "the chaperone" activity and assist the formation and secretion of VLDL particles [86]. According to such a theory, the impacts of sortilin on liver lipid metabolism depend on the physiological demands and the metabolic context. Moreover, sortilin can target lipid-related proteins and regulate their expression and functions, consequently influencing lipid metabolism. Thus, it is essential to consider whether deficiency or overexpression of the SORT1 gene or sortilin protein disrupts the expression of other lipid genes and corresponding proteins. Corrected: These contradictory reports regarding the sortilin function in lipid metabolism may result from variations in employed animal models or lipid metabolic milieu. Once the intracellular level of apoB-100 is elevated, sortilin may primarily act as "the degrader," whereby sortilin can target VLDL to the lysosomal degradation and thus reduce the secretion of VLDL particles [28]. Oppositely, in situations of reduced expression of apoB-100, like in the DKO mouse model, sortilin can also exhibit "the chaperone" activity and assist the formation and secretion of VLDL particles [36]. According to such a theory, the impacts of sortilin on liver lipid metabolism depend on the physiological demands and the metabolic context. Moreover, sortilin can target lipid-related proteins and regulate their expression and functions, consequently influencing lipid metabolism. Thus, it is essential to consider whether deficiency or overexpression of the SORT1 gene or sortilin protein disrupts the expression of other lipid genes and corresponding proteins.