5 Conclusion
Cardiovascular diseases have been seriously endangering the physical and mental health of the elderly people(Zhou et al., 2019), and now they are particularly prominent with the aging epidemic. Cardiac lipid metabolism remodeling plays a key role in cardiovascular system diseases including ischemia-reperfusion, diabetic cardiomyopathy, and cardiac hypertrophy(D’Souza et al., 2016). CD36 is an indispensable molecule in lipid metabolism(Kim and Dyck, 2016). Changes in its synthesis, localization, and function directly affect the energy supply and metabolism of the heart. And studies on CD36 in different diseases suggest that CD36 may be a potential target for treatment. Therefore, the transcriptional activation, post-translational modification and localization changes of CD36 may provide new directions for the treatment of cardiovascular diseases.
Post-translational modifications of CD36 have been studied for nearly 30 years(Asch et al., 1993). The post-translational modifications including phosphorylation, ubiquitination, palmitoylation and glycosylation, accurately regulate the maturation, transport and positioning of CD36(Luiken et al., 2016). Researches in vitro have revealed the impacts of post-translational modification of CD36 in cellular fatty acid uptake in adipocytes(Wang et al., 2019) and muscle cells(Sun et al., 2018), etc. But few demonstrates its importance in cardiovascular system. Whether these modifications of CD36 alter the cellular uptake of fatty acids in myocardium and further influence the cardiac function still remains to be elucidated, and which enzymes mediate these modifications in cardiomyocytes and whether these enzymes are supposed to be the new therapeutic target also need further investigations.
Because fatty acids may also cause excessive lipid accumulation while providing energy(Park et al., 2007; Evans and Hauton, 2016), whether the increase in fatty acids uptake caused by CD36 is good or bad are not consistent under different pathological conditions. In addition to being modulated by CD36, fatty acids in cells are also affected by the rate of mitochondrial aerobic oxidation and the rate of triglyceride synthesis and decomposition(Bjorkegren et al., 2001; Heier and Haemmerle, 2016). Therefore, to evaluate the role of CD36 on the myocardial lipid metabolism, the corresponding mitochondrial aerobic oxidation and triglyceride synthesis also need to be taken into consideration. Since it is not uncommon that more than two pathological factors are combined at the same time, such as diabetics suffering hypertension(Neckar et al., 2012) or myocardial infarction(Cheng et al., 2015), the impact of CD36 on myocardial lipid metabolism and cardiac function is definitely more complicated in that case. So, further researches also need to investigate these situations.