Figure 2.

The figure illustrates the role of UCP2/3 to protect cardiomyocytes from LCFA (long chain fatty acid) accumulation in mitochondria and from lipotoxicity induced by increased TGs (triglycerides) and FFAs (free fatty acids) influx to cell. The downregulation of UCPs and SIRT3 and the hyperacetylation of LCAD (long chain acyl-CoA dehydrogenase) and β-HAD (β-hydroxyacyl-CoA dehydrogenase) lead to the accumulation of LCFA-CoA. Nevertheless MTE1 (mitochondrial acyl-CoA thioesterase-1) liberates free CoA required for continued fatty acid oxidation together with LCFA anion which is exported by UCP2/3 outside mitochondria for its activation by ACS (acyl-CoA synthetase) to comeback mitochondria for the β-oxidation. A downregulation of UCP2/3 and MTE1 may result in LCFA accumulation in the matrix and mitochondria dysfunction.