A century of cholesterol and coronaries: from plaques to genes to statins

Cell. 2015 Mar 26;161(1):161-172. doi: 10.1016/j.cell.2015.01.036.


One-fourth of all deaths in industrialized countries result from coronary heart disease. A century of research has revealed the essential causative agent: cholesterol-carrying low-density lipoprotein (LDL). LDL is controlled by specific receptors (LDLRs) in liver that remove it from blood. Mutations that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise LDLRs reduce LDL and diminish heart attacks. If we are to eliminate coronary disease, lowering LDL should be the primary goal. Effective means to achieve this goal are currently available. The key questions are: who to treat, when to treat, and how long to treat.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / drug therapy
  • Cardiovascular Diseases / genetics
  • Cardiovascular Diseases / pathology
  • Cholesterol / metabolism*
  • Coronary Vessels / metabolism
  • Coronary Vessels / pathology*
  • Dietary Fats / metabolism
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*
  • Plaque, Atherosclerotic / drug therapy*
  • Plaque, Atherosclerotic / genetics
  • Plaque, Atherosclerotic / metabolism
  • Receptors, LDL / metabolism


  • Dietary Fats
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Receptors, LDL
  • Cholesterol