Ferroptosis, a form of non-apoptotic cell death that requires iron, has been implicated in various human diseases, however, its mechanisms have not to date been well-defined. Investigators at MSK have identified novel molecular components of ferroptosis as well as mechanisms for ferroptosis regulation. Their findings include the discovery that glutaminolysis is an essential component of ferroptosis.
MSK’s investigators have determined that targeting glutaminolysis can inhibit ferroptosis and by so doing, reduce heart injury triggered by ischemia-reperfusion. Therapeutic strategies aimed at preventing ferroptosis through glutaminolysis inhibition may also prove effective with other types of ischemia-related organ injuries.
- Compelling in vivo results, with implications for a leading global cause of illness and death
- Clinical trials involving a number of compounds aimed at preventing ischemia-reperfusion injury so far have proven disappointing
There is a high unmet need for effective therapies to reduce or prevent myocardial ischemia-reperfusion injury, a leading cause of coronary heart disease. CHD, which is the most common form of heart disease, results in the death of more than 370,000 people annually in the U.S.
U.S. Provisional Patent application filed in May, 2015
Xeujun Jiang, PhD, Laboratory Head, Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering