Novel Bullet for Dyslipidemia and Cardiovascular Disease in the Horizon: Does Genetics Contribute to the Blueprint?
AbstractThe development of novel therapy for dyslipidemia and cardiovascular diseases (CVD) had been constrained by some challenges, and several recent approaches have failed for lack of efficacy. Progress had been made by a single, greatest contribution from statins in reducing the risk of CVD. However, the burden of CVD and residual risk remains quite high, and new pathways to prevent and treat the diseases are still needed. Despite this clear unmet need, nevertheless many research institutions have begun to withdraw their efforts in discovering ‘the new bullet’ for this prevalent diseases1.
2. George M, Selvarajan S, Muthukumar M, Elangovan S. Looking into the Crystal Ball – Upcoming Drugs for Dyslipidemia. J of CardiovascPharmacol Therapeutics 2015; 20(1): 11 – 20.
3. Boden WE, Probstfield JL, Anderson T, et al. AIM-HIGH investigators. Niacin in patients with low-HDL cholesterol levels receiving intensive statin therapy. N Eng J Med 2011; 365: 2255 – 67.
4. Haynes R, Jiang L, Hopewell JC, et al. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25,673 high-risk patients of ER niacin/laropirant: Trial design, pre-specified muscle and liver outcomes and reasons for stopping study treatment. Eur Heart J 2013; 34: 1279 – 91.
5. Schwartz GG, Olsson AG, Ballantyne CM, et al. Effects of dalcetrapib in patinets with a recent acute coronary syndrome. N Eng J Med 2012; 367: 2089 – 99.
6. Nicholls SJ, Kastelein JJ, Schwartz GG, et al. VISTA-16 Investigators. Varespladib and cardiovascular events in patients with an acute coronary syndrome: The VISTA-16 randomized clinical trial. J Am Med Assoc 2014; 311: 252 – 62.
7. White HD, Held C, Stewart R, et al. STABILITY Investigators. Darapladib for preventing ischemic events in stable coronary heart disease. N Eng J Med 2014; 370: 1702 – 11.
8. Plenge RM, Scolnick EM, Altshuler D. Validating therapeutic targets through human genetics. Nat Rev Drug Discover 2013; 12: 581 – 94.
9. Sun H, Samarghandi A, Zhang N, et al. Proprotein convertase subtilisin/kexin type 9 interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor. ArteriosclerThrombVasc Biol. 2012;32(7): 1585 - 95.
10. Shen L, Peng H, Xu D, et al. The next generation of novel low density lipoprotein cholesterol lowering agents: proprotein convertase subtilisin/kexin 9 inhibitors. Pharmacol Res 2013; 73: 27 – 34.
11. Popp Switzer M, Nwosu AC, San Juan Z, et al. Propetein convertase subtilisin/kexin type 9 (PCSK9) and LDL lowering in the contemporary management of dyslipidemia. Cardiovasc Hematol Agents Med Chem2013; 11(4): 281 – 8.
12. Cohen JC, Boerwinkle E, Mosley TH, et al. Sequence variations in PCSK9, low LDL and protection against coronary heart disease. N Eng J Med 2006; 354: 1264 – 72.
13. Stein EA. Low density lipoprotein cholesterol reduction by inhibition of PCSK9. CurrOpinLipidol 2013; 24: 510 – 17.
14. Pollin TI, Damcott CM, Shen H, et al. A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection. Science 2008; 322: 1702 – 05.
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