A new research trial has discovered a cell mechanism that could lead to the explanation of why smoking, alcohol, and other modifiable factors could increase the risk of developing a rare bone disease known as osteoporosis.
According to the experts involved in the discovery, the mechanism spurs are a cell type located in the immune system that turns into osteoclasts, which are a type of cell that resorbs, or dissolves, bone.
They found that the mitochondria, the tiny holes that are responsible for producing energy in cells, send out a signal that sparks this process when they are under stress.
They explained that when this happens, the mitochondria of macrophages turn into the osteoclasts. Macrophages are defined as prolific immune cells that remove cell waste and foreign objects by digesting them or swallowing.
Experts in charge of conducting the studies all attending the University of Pennsylvania (Penn) in Philadelphia and the Icahn School of Medicine at Mount Sinai in the city of New York. The team published their discoveries in the recent FASEB Journal study paper.
“We show in this paper that when mitochondrial function is affected, it not only affects energy production but also triggers a type of stress signaling that induces the overproduction of osteoclasts,” noted senior study author Narayan G. Avadhani, currently a professor of biochemistry at Penn’s School of Veterinary Medicine.
They noted that environmental factors, which include smoking, drinking alcoholic drinks, and taking certain medications, that will impair the functions of the mitochondria, seem to increase the risk of osteoporosis
According to Prof. Avadhani and a team of researchers claim that the stress signaling pathway that they unearthed could be the main reason. Osteoporosis is a condition that will cause bones to become less dense and more porous and brittle, which heightens the risk of a break or fracture.
Over time as people age, their risk of developing osteoporosis increases. They suggest that this is due to the balance between the bone generation and bone restoration shifts with age.
Typically when people reach their 30’s, the bone density is at its highest. From then on, their bones decline with a density as the balance gradually favors resorption over generations.
The International Osteoporosis Foundation (IOF) report that “1 in 3 women and 1 in 5 men over the age of 50 will experience a bone fracture due to osteoporosis.”
The IOF additionally estimates that approximately 75 million people in the United States, Europe, and Japan have the condition and that osteoporosis will be the cause of more than 8.9 million bone fractures per year around the world.
The team noted in her paper, that the mitochondria-to-nucleus retrograde signaling (MtRS) pathway that aids other cells to adapt to the growing stress.
“However,” they note, “mechanisms through which macrophages sense and respond to cellular stress remain unclear.”
To test how mitochondrial damage might be involved, they conducted other trials laboratory-cultured mouse macrophages. The team caused havoc in the macrophages by disrupting an enzyme called cytochrome oxidase C, known to regulate mitochondrial energy production.
As a result, the macrophages released various signaling molecules that induced inflammation but also caused the cells to differentiate into osteoclasts.
With more experimentation, they found that something was happening with another molecule called RANK-L. They explained how the Bone-generation releases RANK-L, which spikes the bone resorption. They noted that this helps maintain the balance between the two processes.
The team suggests that when the damaged mitochondria sent out signals, macrophages continued to differentiate into osteoclasts and as a downfall promote bone resorption-even if there wasn’t enough RANK-L around.
To conclude their trials, the final set of tests in a mouse model of mitochondrial dysfunction confirmed the discoveries.
As a result, the team is urging others to conduct further studies to find out if preserving the mitochondrial function could decrease the risk of osteoporosis.
“In some respects, mitochondrial stress signaling may even be replacing RANK-L. That we don’t know now, but we plan to look into that further.”
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