Good news! Closing in on the fountain of youth!
"... there’s a powerful new way to slow or even halt that deterioration, and it lies inside extracellular vesicles. Those are tiny, membranous particles, ranging from 10 microns down to 20 nanometers, that exit cells and dwell in the spaces among them.
In their ... paper “Embryonic stem cell-derived extracellular vesicles delay cellular senescence by inhibiting oxidative stress,” ... explore how extracellular vesicles from embryonic stem cells can protect other cells from oxidative stress. ..."
From the abstract:
"The accumulation of cells that permanently exit the cell cycle and undergo senescence is a hallmark of aging and predisposes organisms to disease.
Emerging evidence suggests extracellular vesicles (EVs) released by pluripotent embryonic stem cells (ESCs) possess therapeutic/regenerative properties with the potential to significantly impact cellular senescence and aging-related disorders. However, the critical next step for taking advantage of the potential benefits offered by ESC-derived EVs will be to unravel the molecular mechanisms responsible for their unique functional effects, which thus far have not been fully defined.
Toward that goal, we now identify a signaling pathway essential for EVs shed by ESCs to potently block fibroblasts and astrocytes from undergoing senescence.
It starts with the extracellular matrix protein fibronectin that coats the surfaces of EVs, enabling the vesicles to bind integrins on cells and trigger the activation of FAK and AKT. This leads to the inhibition of GSK3β activity and stabilization of the transcription factor Nrf2, which counteracts the effects of oxidative stress that would otherwise drive cellular senescence.
These findings define a signaling pathway used by ESC-derived EVs to extend cellular lifespan, highlighting their potential application in anti-aging strategies."
Embryonic stem cell-derived extracellular vesicles delay cellular senescence by inhibiting oxidative stress (open access)
Figure 8 Diagram showing how EVs produced by pluripotent ESCs delay cellular senescence. The MVs and exosomes produced by ESCs are coated with fibronectin, which can engage and activate integrins expressed in target cells. This results in the activation of a signaling pathway that inhibits GSK3β, increases the stability of Nrf2, and suppresses the accumulation of ROS that would otherwise trigger cells to undergo senescence.
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