CD36, a scavenger receptor, plays an important role in the progression of atherosclerosis through its interaction with oxidized low-density lipoprotein (ox-LDL).
CD36 has been reported to participate in atherosclerosis process and miR-135a mimics can inhibit its expression while miR-135a inhibitors exhibited a reverse phenomenon.
Accordingly, paeonol retarded the progress of atherosclerosis in ApoE(‑/‑) mice and modulated the expression of CD36 and ABCA1 in aortas similarly to that observed in macrophages.
Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis.
All of these results demonstrated that FSTL3 as a novelty cytokine takes part in the process of atherosclerosis through increasing lipid accumulation and inflammation through regulating CD36 and LOX-1 expression.
Azapeptide analogues of growth hormone-releasing peptide-6 (His-d-Trp-Ala-Trp-d-Phe-Lys-NH<sub>2</sub>, GHRP-6) have for example been pursued as ligands of the cluster of differentiation 36 receptor (CD36) and show promising activity for the development of treatments for angiogenesis-related diseases, such as age-related macular degeneration, as well as for atherosclerosis.
Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.
Correlation between the anti-CD36 activity of these inhibitors and the known pathophysiological activity of this scavenger receptor in the development of atherosclerosis and diabetes were observed at pharmacological doses.
During foam cell formation and atherosclerosis development, the scavenger receptor CD36 plays critical roles in lipid uptake and triggering of atherogenicity via the activation of Vav molecules.
EP80317 is an hexapeptide that serves as a ligand for CD36 and features protective effects under conditions such as atherosclerosis and vascular inflammation.
Functionally, MT4-MMP-null Mafb+AIM+ peritoneal macrophages express higher AIM and scavenger receptor CD36, are more resistant to apoptosis, and bind acLDL avidly, all of which contribute to atherosclerosis.