Fig. 2

Two possible antagonistic effects of Mitochondria contact LDs. A DGAT2 was found to co-localize with the attachment of lipid droplet surface and mitochondria, and it may play a role in facilitating the binding of LDs to mitochondria. B Perilipins are LD-scaffolding proteins, PLIN-5 recruits mitochondria to the LD surface through a C-terminal region, while down-regulation of PLIN-5 expression reduces the contact of mitochondria with LDs. C MIGA2 is an outer mitochondrial membrane protein that can link mitochondria to LDs through a specific region of its C terminus. D Mitochondria anchored to LDs exhibit reduced motility and fission, the specific interaction between PLIN1 and MFN2 may promote mitochondria–LDs interaction by enhancing cellular responsiveness to lipolysis. In addition to that, the knockdown of MFN1 and OPA1 resulted in the separation of mitochondria with LDs. E Marf is required to be in contact with LDs to store cholesterol, neuronal cholesterol reduction induces p-Tau degradation by enhancing proteasome levels and increasing total cellular proteasome activity. F Underfed conditions, lipolysis is activated by LD-associated lipases, such as ATGL, HSL, and MGL, which promote the breakdown of TAG to FAs. Then, FAs are transported to mitochondria for β-oxidation