So, de Gray gave that mechanism for ROS export (which I think was one of his best contributions on the theory side of things, it was plausible and well-grounded and quite novel). It is a mechanism which can happen, although I don’t know of experimental evidence for whether it’s the main mechanism for ROS export, especially in senescent cells. And that also still leaves the question of ROS import into other cells—not so relevant for atherosclerosis, but quite relevant to the exponential acceleration of aging. Also, it leaves open the question of ROS transport between mitochondria/cytoplasm/nucleus, which is necessary to explain the DNA damage part of the senescence feedback loop.
Great comment.
So, de Gray gave that mechanism for ROS export (which I think was one of his best contributions on the theory side of things, it was plausible and well-grounded and quite novel). It is a mechanism which can happen, although I don’t know of experimental evidence for whether it’s the main mechanism for ROS export, especially in senescent cells. And that also still leaves the question of ROS import into other cells—not so relevant for atherosclerosis, but quite relevant to the exponential acceleration of aging. Also, it leaves open the question of ROS transport between mitochondria/cytoplasm/nucleus, which is necessary to explain the DNA damage part of the senescence feedback loop.