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Rescuing Senescent Cells by Delivering New Mitochondria Sounds Like a Risky Proposition

Rescuing Senescent Cells by Delivering New Mitochondria Sounds Like a Risky Proposition
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Mitochondria are effectively power plants, hundreds of these organelles per cell working to create the chemical energy store molecule adenosine triphosphate. Mitochondria are the descendants of ancient symbiotic bacteria, and retain many bacterial characteristics, including a small genome, the mitochondrial DNA, and the ability to replicate. Mitochondrial dysfunction is one of the paths by which cells can become senescent, entering a state of growth arrest while secreting an inflammatory set of signals, but mitochondria are in any case involved in the transition to senescence in response to other forms of damage or dysfunction. In youth, senescent cells are quickly destroyed by their own programmed cell death processes or by the immune system. In older people, these cells accumulate, contributing to tissue dysfunction and the chronic inflammation of age.

Mitochondriaorganellesadenosine triphosphategenomemitochondrial DNAMitochondrial dysfunctionone of the pathsinvolved in the transitionprogrammed cell deathimmune systemchronic inflammation

In today’s open access paper, the authors propose treating skin aging by delivering whole mitochondria into senescent cells, thereby rescuing their function. In recent years, various approaches to introducing mitochondria into target cells have been demonstrated. It also appears to be the case that cells naturally transfer, eject, and ingest mitochondria under a range of circumstances. Is

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