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.