Fig. 2

How lipoproteins are broken down in reaction to treatments that target PCSK9. Antisense oligonucleotides (ASOs) attach to the PCSK9 mRNA and stop it from being made. 2. Small interfering RNAs (siRNAs) stop the production of PCSK9 by encouraging the breakdown of PCSK9 mRNA. 3. Small molecule inhibitors stop PCSK9 from activating and being released from the ER, which is an essential step in the maturation process. 4. LDLR can’t connect with PCSK9 because of small peptides that look like the structure of PCSK9’s catalytic domain, C-terminal domain, or epidermal growth factor precursor homology domain-A. 5. Bancovirus monoclonal antibodies stop PCSK9 from attaching to LDLRs. Therapies that target PCSK9 improve the clearance of LDL particles through receptors by stopping LDLRs from breaking down. This encourages LDLR to return to the cell surface. Proteins that are special to PCSK9 and create higher-than-normal amounts of LDLRs may help explain why treatment causes lower levels of lipoprotein(a) (Lp(a)). A recent study backs up this theory [23, 24]