University of Texas, Houston TX, and Brigham and Women’s Hospital, Harvard University, Boston MA Researchers: Sudhir Paul, Yasuhiro Nishiyama, Stephanie Planque (University of Texas); Brian O’Nuallain (Brigham and Women's Hospital, Harvard Medical School)
Albert Einstein College of Medicine (AECOM), Bronx NY Researchers: Jan Vijg, Silvia Gravina
Researchers: Pedro Alvarez, Jacques Mathieu, Jason Gaspar
Our arteries slowly stiffen with age, in substantial part because of chemical crosslinking of their structural proteins by blood sugar and other fuels in the circulation. Like the crosslinking that causes rubber windshield wipers to become stiff and brittle over time, the crosslinking of arterial proteins with age leaves us with increasingly rigid blood vessels...
Researchers: Haroldo Silva, David Halvorsen, Kelsey Moody, Thomas Hunt
Researchers: Matthew O'Connor, Amutha Boominathan, Jayanthi Vengalam
Researchers: Gouri Yogalingam, Ghezal Beliakoff, Ehud Goldin, Maximus Peto
We all know that mitochondria are the cell's "powerhouse" for energy. One interesting fact about these organelles is that they have their own DNA in addition to the nuclear DNA that we are all aware of. However, the mitochondrial DNA is prone to mutations due to constant exposure from reactive oxygen species because it is not encased in a nuclear envelope nor does it have efficient repair mechanisms to correct mutations as they occur. Amutha Boominathan explains how moving the mitochondrial genes to the nucleus, where it's safer to express them for function, would let mitochondria keep producing energy normally, even after mitochondrial mutations have occurred.
Jayanthi Vengalam explains her work with the Mitochondrial Mutation team, with consequences for acute diseases such as diabetes, Parkinson's and Alzheimer's