Research Alert
Rockville, Md. (February 3, 2022)—Enabling the timely activation of the mitochondrial ATP channel can significantly reduce the size of a heart attack or stroke by turning on key signals inside cells to protect critical and sensitive targets against damage, according to a new study published ahead of print in the journal Function. The new findings also show that certain natural proteins in our bodies that promote cell survival, and certain drugs and compounds that activate the opening of a specific kind of K+ channels that can have the same cell-protective benefits, can upregulate the efficiency of ATP synthase, increasing its ability to make ATP for a given amount of H+ and K+ driving force. This action also enables the mitochondria to accumulate K+ in parallel fashion with this activation, mimicking the functions and activation of a separate K+ channel thought to exist called the mitochondrial ATP-dependent K+ channel. Understanding these mechanisms should lead to better therapeutic approaches to limit the damage of heart attacks and strokes, and to the better management of problems involving impaired energy homeostasis, such as in advanced heart failure and as accompanies aging and frailty.
Read the full article, “ATP synthase K+- and H+-fluxes drive ATP synthesis and enable mitochondrial K+-“uniporter” function: II. Ion and ATP synthase flux regulation,” published ahead of print in Function. Contact APS Media Relations or call 301.634.7314 to schedule an interview with a member of the research team.