Fig. 8. Schematic figure illustrating that the RTN3-mediated LD biogenesis in cardiomyocytes.

Under lipid overload conditions, C/EBPα was upregulated, which then activated the transcription of RTN3. The increased RTN3 interacted with FABP5 in ER membrane and facilitated the transportation of FA to ER, thereby promoting LDs biogenesis. Moreover, DGAT2 was the key enzyme responsible for this process, which colocalized with RTN3 around LD. The pathologically activated RTN3-mediated LD biogenesis led to LD increase in cardiomyocytes and myocardial lipid accumulation. C/EBPα CCAAT/enhancer binding protein α, RTN3 reticulon 3, ER endoplasmic reticulum, DGAT2 diacylgycerol acyltransferase 2, FABP5 fatty acid binding protein 5, FA fatty acids, LD lipid droplet.