Scientists at Temple University Lewis Katz School of Medicine have discovered a new protein that may help protect the heart and brain from damage caused by calcium overload in cells.
The protein, called TMEM65, plays a key role in helping cells remove calcium from their energy centers, known as mitochondria.
This discovery could lead to new treatments for serious diseases such as heart failure and Alzheimer's disease.
Within our cells, mitochondria produce the energy that keeps the body working.
For this process to work well, the mitochondria must have the right amount of calcium.
If too much calcium builds up, it can cause damage and even lead to cell death.
This is especially dangerous for the heart in heart attacks and for the brain in diseases such as Alzheimer's.
To control calcium levels, cells use a protein called NCLX, which removes extra calcium from the mitochondria. Until now, scientists did not fully understand how NCLX is regulated and which other proteins help it work.
In this new study, researchers found that TMEM65 works with NCLX and is necessary for its proper functioning. When TMEM65 is missing, calcium builds up to harmful levels.
Dr. John W. Elrod, the study's principal investigator, explained that for the first time a true partner of NCLX has been identified. TMEM65 was discovered through a special method in which researchers tagged the NCLX protein with a marker to see which other proteins interacted with it.
One of the key researchers, Dr. Joan Garbinzius, created a version of NCLX that tags nearby proteins. This helped the team to discover TMEM65.
The study shows that when TMEM65 is removed from cells, the mitochondria cannot get rid of excess calcium, leading to damage. In mice with low levels of TMEM65, this leads to serious problems with muscle movement and control as they age.
This discovery confirmed how important TMEM65 is in maintaining healthy calcium levels in NCLX.
Since calcium overload is a problem in many diseases, finding a way to control it can be very helpful. Dr. Elrod and his team now plan to investigate whether regulating TMEM65 activity can be used as a treatment. They believe this protein could be a powerful target for future drugs.
This work has already been recognized by the scientific community. In 2024, Dr. Garbinzius received a major award from the American Heart Association for his role in the discovery. According to the school's dean, Dr. Amy Goldberg, this research is a great example of how basic science can lead to real solutions to major health problems. | BGNES
