Two papers in the Journal of Nature and Aging Cell: How Mitochondrial Dysfunction Contributes to Premature Aging and Disease

Researchers at the University of Buffalo and their collaborators have developed powerful new ways to study and possibly reverse the cellular mechanisms

Mitochondria provide most of the energy a cell needs to function properly, so genetic defects in the mitochondria can lead to serious diseases that can be devastating if not detected and treated

But exactly how these mitochondrial defects cause disease and aging are not well understood

Mitochondria and telomeres

The Senescent Cells paper is the first to link mitochondrial dysfunction to telomere shortening, a key biomarker of

Professor Taosheng Huang, MD, Chair of the Department of Pediatric Genetics at the Jacobs School of Medicine and Biomedical Sciences at the University of Buffalo, explains: "Telomeres are special DNA sequences that serve as a hat that stabilizes the ends of chromosomes

"Telomere shortening is often considered an important biomarker of aging, but for a long time, no one knew its mechanism

The experiment was conducted with a mouse model called Porg "mutator," which carries a specific genetic defect that can accelerate the rate of mitochondrial DNA mutations

Professor Taosheng Huang said: "We were also able to demonstrate in humans how a change in a nucleotide in mitochondrial DNA accelerates aging, which is associated

The paper shows for the first time that in this model, mitochondrial DNA mutations produce faster aging, which, as the DNA clock shows, estimate a person's biological age

The study is the result of a successful collaboration between all authors, including Steve Horvath, Ph.

The study was funded by the National Institute of Environment and Occupational Health and the National Institute on Aging, both of which are National Institutes of

Interactions between tissue cells

On July 25, the journal Nature Communications published a paper revealing how optogenetics uses light to manipulate cellular activity, and it can be used not only as a research tool, but also as a tool to coordinate organelle interactions in real time

The paper focuses on mitochondrial dynamics, a process that these organelles constantly undergo to maintain a healthy balance

Taosheng Huang said, "In the nature communications paper, we describe a technique we developed that for the first time allows us to directly manipulate the interactions between mitochondria and other organelles in the cell.

"By using optogenetics to force a physical action between mitochondria and another cellular component, lysosomals, we are able to restore mitochondria to a more normal size while improving their energy production function, and we believe this new finding could serve as a basis for future diagnosis and treatment of

The work was made possible by using a powerful imaging technique at the University of Cincinnati, the Structural Illumination Microscope (SIM), which Huang began before the University of Cincinnati became a current researcher

Taosheng Huang is an expert in the genetics of mitochondrial diseases who has pioneered pioneering innovations in the detection and treatment of genetic diseases
.
He was recruited from Cincinnati Children's Hospital Medical Center to UB and John R.
Oishei Children's Hospital
in 2020.
He is also the Medical Director of the Department of Genetics and Metabolism at orsay Children's Hospital and the Director of Human Genetics of the Department of Pediatrics at
UBMD.

The co-authors of the paper in the journal Nature Communications are from the University of Cincinnati School of Medicine, Cincinnati Children's Hospital Medical Center, and the University of Illinois at Urbana-Champaign
.
The study was funded
by the National Institutes of Health.

Article title

Premature aging is associated with higher levels of 8-oxoguanine and increased DNA damage in the Polg mutator mouse