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In a mouse model developed at the University of Alabama in Birmingham, Keshav Singh, Ph.D., and his colleagues found when a shift leading to mitochondrial dysfunction is induced; the mouse develops a wrinkled skin and a loss of hair extended and visible in a few weeks.
When mitochondrial function is restored by disabling the gene responsible for mitochondrial dysfunction, the mouse returns to the smooth skin and thick fur, indistinguishable from an important one, the mutation that triggers this is in a nuclear gene affecting mitochondrial function, the tiny organelles known as the central cells.
In humans, a decline in mitochondrial function is seen during aging, and mitochondrial dysfunction can lead to age-related diseases.
A depletion of DNA in mitochondria is also implicated in human mitochondrial diseases, cardiovascular disease, diabetes, age-related neurological disorders, and cancer. the mouse model is induced when doxycycline antibiotic is added to food or drinking water. This causes the depletion of mitochondrial DNA because the enzyme to replicate the DNA becomes inactive.
In four weeks, mice showed gray hair, reduced hair density, hair loss, slow movement and lethargy. Dramatically, this hair loss and wrinkled skin could be reversed by disabling the mutation.
Little change was observed in other organs when the mutation was induced, suggesting an important role for mitochondria in the skin compared to other tissues. Wrinkled skin has shown changes similar to those seen in intrinsic and extrinsic aging – intrinsic aging is the natural process of aging, and extrinsic aging is the effect of external factors that influence aging, such as wrinkles of the skin
Inversion of the mutation restores mitochondrial function, as well as cutaneous and capillary pathology. This has shown that mitochondria are reversible regulators of skin aging and hair loss, an observation that Singh calls "surprising".
Source: ANI
Source of the Image: Shutterstock [19659002]
Posted: 23 July, 2018 07:58 | Last Updated: July 23, 2018 8:05
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