|
|
| Name |
Marks, Andrew R. |
| Location
|
Columbia University College of Physicians and Surgeons |
| Primary Field
|
Medical Physiology and Metabolism |
| Secondary Field
|
Physiology and Pharmacology |
 Election Citation
|
|
Marks revolutionized cardiac therapy when he showed that rapamycin inhibits proliferation and migration of vascular smooth muscle cells and prevents coronary artery stenosis. He subsequently developed the first drug-eluting coronary artery stent, which significantly reduced restenosis rates and has prolonged many lives. |
|
Research Interests
|
|
Marks' identification of the mechanism of action of rapamycin's inhibition of vascular smooth muscle proliferation and migration lead to the development of the first drug-eluting stent (coated with rapamycin) for treatment of coronary artery disease. This substantially reduced the incidence of in-stent restenosis. Marks reported the high resolution structure of the mammalian type 1 ryanodine receptor/calcium release channel (required for excitation-contraction coupling in skeletal muscle) which he cloned and defined it's regulation in health and disease. His research has contributed new understandings of fundamental mechanisms that control muscle contraction, heart function, lymphocyte activation, and cognitive function. He discovered that "leaky" intracellular calcium release channels (ryanodine receptors) contribute to heart failure, fatal cardiac arrhythmias, impaired exercise capacity in muscular dystrophy, post-traumatic stress disorder (PTSD) and Alzheimer's Disease. Marks discovered a new class of small molecules (Rycals), developed in his laboratory, that target leaky ryanodine receptor channels and effectively treat cardiac arrhythmias, heart failure, muscular dystrophy and prevent stress induced cognitive dysfunction and symptoms of Alzheimer's Disease in pre-clinical studies. Rycals are now in clinical trials for the treatment of heart failure and cardiac arrhythmias, and entering clinical trials for the treatment of Duchenne Muscular Dystrophy. |
|
|
|