Long-chain acyl-CoA synthetase (ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form acyl-CoAs, which are lipid metabolic intermediates and involved in fatty acid metabolism, membrane modifications and various physiological processes. Gain- or loss-of-function studies have shown that the expression of individual ACSL isoforms can alter the distribution and amount of intracellular fatty acids. Changes in the types and amounts of fatty acids, in turn, can alter the expression of intracellular ACSLs. ACSL family members affect not only the proliferation of normal cells, but the proliferation of malignant tumor cells. They also regulate cell apoptosis through different signaling pathways and molecular mechanisms. ACSL members have individual functions in fatty acid metabolism in different types of cells depending on substrate preferences, subcellular location and tissue specificity, thus contributing to liver diseases and metabolic diseases, such as fatty liver disease, obesity, atherosclerosis and diabetes. They are also linked to neurological disorders and other diseases. However, the mechanisms are unclear. This review addresses new findings in the classification and properties of ACSLs and the fatty acid metabolism-associated effects of ACSLs in diseases.

Porcine aortas may prove to be useful ex-vivo models in the study of aortic dissection haemodynamics. These models are reproducible and may be used in the study of complex haemodynamic forces during the development and propagation of TBAD. Our three porcine models give a potential possibility in helping clinicians isolate and analyse complex haemodynamical factors in the development, propagation and prognosis of TBAD.

Aortic remodeling after TEVAR in chronic dissection is a continuous process. There were no significant differences between chronic dissections and aneurysms in all volumetric parameters. Treating chronic dissections early, before aneurysm formation, did not appear to have a morphologic advantage.