I am a scientist, businessman, author, and philanthropist. For nearly two decades, I was a professor at Harvard Medical School and Harvard School of Public Health where I founded two academic research departments, the Division of Biochemical Pharmacology and the Division of Human Retrovirology.
Cells, like us humans, grow old with time. As they do, they begin to secrete inflammatory molecules. A little inflammation is important for wound healing and for fighting infections, but it needs to be “turned off” again afterward, otherwise it begins to damage the very thing it set out to heal. Why old cells cause inflammation is not fully understood. Now, researchers at the University of Glasgow and at the Mayo Clinic may have found an answer.
In the case of senescent cells, there seems to be a breakdown of this process. The researchers discovered that they are instead characterized by a kind of “” . Essentially, some of the mitochondria in the cell begin to undergo outer membrane permeabilization while others do not. The end result is an extended in-between phase of inflammation: too little MOMP to cause cell death, but too much MOMP to allow for healthy functioning of the cell.
The team of scientists noticed that, in senescent cells undergoing outer membrane permeabilization, mitochondrial DNA “leaks” into the cytoplasm of the cells. This misplaced DNA causes alarm bells to ring, leading to the activation of a major mediator of inflammation, known as the cGAS–STING signaling pathway.Having isolated one of the mechanisms behind the senescence-associated secretory phenotype , the researchers set out to intervene.
The role of the mitochondria in inducing aging via inflammation is yet another dysregulations associated with aging. In due time, this new understanding will lead to drugs that slow the process. That, together with knowledge of other pathways that go awry as we age, will lead to longer, healthier lives.
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