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10.2147/DDDT.S36984

http://scihub22266oqcxt.onion/10.2147/DDDT.S36984
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24115837!3793591!24115837
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suck abstract from ncbi


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pmid24115837      Drug+Des+Devel+Ther 2013 ; 7 (ä): 1135-48
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  • The biology of PCSK9 from the endoplasmic reticulum to lysosomes: new and emerging therapeutics to control low-density lipoprotein cholesterol #MMPMID24115837
  • Poirier S; Mayer G
  • Drug Des Devel Ther 2013[]; 7 (ä): 1135-48 PMID24115837show ga
  • Proprotein convertase subtilisin/kexin type 9 (PCSK9) directly binds to the epidermal growth factor-like repeat A domain of low-density lipoprotein receptor and induces its degradation, thereby controlling circulating low-density lipoprotein cholesterol (LDL-C) concentration. Heterozygous loss-of-function mutations in PCSK9 can decrease the incidence of coronary heart disease by up to 88%, owing to lifelong reduction of LDL-C. Moreover, two subjects with PCSK9 loss-of-function mutations on both alleles, resulting in a total absence of functional PCSK9, were found to have extremely low circulating LDL-C levels without other apparent abnormalities. Accordingly, PCSK9 could represent a safe and effective pharmacological target to increase clearance of LDL-C and to reduce the risk of coronary heart disease. Recent clinical trials using anti-PCSK9 monoclonal antibodies that block the PCSK9:low-density lipoprotein receptor interaction were shown to considerably reduce LDL-C levels by up to 65% when given alone and by up to 72% in patients already receiving statin therapy. In this review, we will discuss how major scientific breakthroughs in PCSK9 cell biology have led to the development of new and forthcoming LDL-C-lowering pharmacological agents.
  • |Animals[MESH]
  • |Antibodies, Monoclonal/pharmacology[MESH]
  • |Anticholesteremic Agents/*pharmacology[MESH]
  • |Cholesterol, LDL/*blood[MESH]
  • |Coronary Disease/physiopathology/prevention & control[MESH]
  • |Drug Design[MESH]
  • |Endoplasmic Reticulum/metabolism[MESH]
  • |Humans[MESH]
  • |Lysosomes/metabolism[MESH]
  • |Molecular Targeted Therapy[MESH]
  • |Mutation[MESH]
  • |Proprotein Convertase 9[MESH]
  • |Proprotein Convertases/antagonists & inhibitors/genetics/*metabolism[MESH]
  • |Receptors, LDL/metabolism[MESH]


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