Solve the decades-old mystery Scientists have discovered for the first time the key mitochondrial protein in human cells

Recently, the top academic journal Nature in the form of "accelerated preview" of a research paper, caused a lot of attention.
scientists have identified mitochondrial NAD-transport proteins in human cells for the first time.
findings not only solve the mysteries that have plagued the scientific community for decades, but also open new doors for treating many of the diseases associated with aging.
mitochondrials are called "power plants" of cells, converting nutrients into the chemical energy of cells.
and mitochondrial-mediated energy production and cellular function, niacin adenine dinucleotides (NAD plus) are essential key molecules.
low levels of NAD plus are signs of aging and are associated with diseases such as muscular dystrophy and heart failure.
although much of the research on NAD plus over the past hundred years has focused on the processes that occur in mitochondrials, it is a long-standing mystery how NAD plus actually goes inside mitochondrials.
scientists have found "transport proteins" in yeast and plant cells that transport NAD-plus from cytostytes into mitochondrials.
but in mammalian cells, no corresponding transport proteins have been found, and even suspect the presence of such molecules.
in this study, the scientists had a clear answer.
tests, they found an unidentified mitochondrial protein, SLC25A51 (also known as MCART1), which has long been sought in mammalian cells.
To confirm the function of this protein, the researchers isolated mitochondrials in human cells and found that the concentration of NAD plus inside mitochondrials increased significantly after increasing SLC25A51;
addition, isotope tradding techniques have shown directly that in these human cells, all NAD-plus in mitochondrials is transported from the cytopyte, rather than synthesized inside the mitochondrial.
In several different cell lines, when SLC25A51 and its family SLC25A52 were expressed, the level of NAD plus in mitochondrials increased, and when SLC25A51 was knocked out, THE levels in mitochondrials decreased significantly (Photo source: References.
" co-author Professor Joseph A. Baur of the University of Pennsylvania said, "This discovery opens up a whole new field of research."
now that we know how NAD plus is transported, we can manipulate it at the subcellular level, selectively consuming or adding this molecule.
" researchers point out that regulating NAD-plus levels can target the treatment of a variety of diseases.
in the past, the inability to precisely target mitochondrial control, increasing or decreasing NAD-plus levels throughout the cellular range, could lead to unexpected changes in gene expression or other types of metabolism.
scientists could develop new treatments with the first discovery of human cell mitochondrial NAD-transport proteins.
For example, many cancer cells rely heavily on the metabolic process of glycolysis, and sugar enzymes and mitochondrial respiration are using NAD plus, activation of transport levels can make cells more biased towards breathing and reduce glycolysis, so that cancer cells at a disadvantage.
, for example, the heart needs a lot of mitochondrial energy to continuously supply blood to the outer tissue.
if mitochondrial absorption of NAD-plus, which specificly regulates myocardial cells, is expected to improve heart failure and may also help boost endurance during exercise.
that while current research is still in its early stages for these applications, new research around mitochondrial NAD-plus and transport protein genes has opened the door.
references to the SLC25A51 is aradian mitochondrial NAD-transporter. Nature. DOI: Penn Researchers Solved Decades Old Mitochondrial Mystery That Lead to New Disease Treatments. Retrieved Sep. 13, 2020, from