Thomas
Nyström, study leader and a researcher in the Department of Cell and Molecular
Biology at the University of Gothenburg,
and a team of researchers, have discovered that a group of mitochondrial
proteins may be responsible for age-related diseases.
Scientists
have theorized that the mitochondria, which are the power stations of cells,
are responsible for human aging. This theory comes from the fact that
mitochondria not only produce the body's energy, but also create harmful byproducts.
These byproducts are reactive oxyradicals, and they attack several other parts
of the cell. When a cell is attacked, it could become permanently damaged,
which forces it to discontinue the operation of important functions. In the
theory's conclusion, the lack of certain functional cells over time causes the
organism to age.
Now,
Nyström and his colleagues have found that these mitochondrial proteins, called
MTC proteins, may play
a crucial role in age regulation in humans. The proteins are
traditionally apart of mitochondrial protein synthesis, but have other roles
that impact genome stability.
"When
a certain MTC protein is lacking in the cell, e.g. because of a mutation in the
corresponding gene, the other MTC proteins appear to adopt a new
function," said Nyström. "They then gain increased significance for
the stabilization of the genome and for combating protein damage, which leads
to increased lifespan.
"These
studies also show that this MTC-dependent regulation of the rate of aging uses
the same signaling pathways that are activated in calorie restriction -
something that extends the lifespan of many different organisms, including
yeasts, mice and primates. Some of the MTC proteins identified in this study
can also be found in the human cell, raising the obvious question of whether
they play a similar role in the regulation of our own aging processes."
While
previous studies have shown that mitochondrial dysfunctions in cells delay
aging in worms, fungi and flies, Nyström hopes to confirm the same in humans by
controlling the mitochondrial proteins, which affect the cell's ability to
remove the harmful proteins.
"It
is possible that modulating the activity of the MTC proteins could enable us to
improve the capacity of the cell to delay the onset of age-related
diseases," said Nyström. "These include diseases related to
instability of the genome, such
as cancer, as well as those related to harmful proteins, such as
Alzheimer's disease and Parkinson's disease. At the moment this is only
speculation, and the precise mechanism underlying the role of the MTC proteins
in the aging process is a fascinating question that remains to be
answered."
This
study was published in Molecular Cell.
