Protein Power
Finding how two proteins conspire to get kidney cells to self-destruct when oxygen supplies are low may one day improve dismal mortality rates for ischemic renal failure, researchers say.
Dehydration, low blood pressure, septic shock, trauma or removing a kidney for transplantation can temporarily halt or reduce blood and oxygen supplies, said Dr. Zheng Dong, a cell biologist.
Ischemia leads to cell suicide, or apoptosis, particularly in the energy-consuming tubular cells of the kidney. Fifty-percent mortality rates from resulting ischemic renal failure haven’t changed in nearly as many years, Dr. Dong said.
Tubular cells—which have the daunting daily task of reabsorbing nearly 50 gallons of usable fluid volume, including salt and glucose the kidneys filter from the blood every 24 hours—are particularly vulnerable to apoptosis and injury, Dr. Dong said.
It’s in this oxygen-deprived environment that two proteins, Bid and Bax—each a known killer in its own right—are activated and may partner to induce cell death. The killing proteins are pervasive, particularly in the kidneys, said Dr. Dong, who recently received a $1 million grant from the National Institute of Diabetes & Digestive & Kidney Diseases, to better understand their role in cell death during ischemic renal failure.