Fig. 2

Schematic model of FITM expression regulation and their functions primarily in the formation and budding of LDs (modified mainly according to references [6, 20, 30, 47]). The expression of FITM1 can be upregulated by MyoD1, PPARα, and PGC-1α, while MyoD1 is activated by the Hippo signaling pathway. The expression of FITM2 is increased by PPARα, and decreased by Zfp69. The overexpression of FITM2 leads to the inhibition of the Wnt/β-catenin pathway and stimulates caveolae formation by regulating the expression of caveolin-1. The process of de novo LD biosynthesis is divided into three major steps: A Neutral lipid synthesis and nucleation; B Budding; C Expansion. During this process, FITM2 might help to concentrate TAG between the leaflets of the endoplasmic reticulum, and then promote the formation of an oil lens structure, which is the characteristic of the nucleation step. In addition, FITM2 maybe participate in reducing the DAG level in the cytoplasmic leaflets, and then facilitate the budding of lipid droplets. Furthermore, FITM2 could bind to cytoskeletal protein Septin7 and interact with ER tubule-forming proteins Rtn4 and REEP5 during nascent LD formation. PGC-1α peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, PPARα peroxisome proliferator activated receptor alpha, MyoD1 myogenic differentiation 1, TAGs triacylglycerols, DAGs diacylglycerols, SEs sterol esters, PA phosphatidic acid