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Ageing in multicellular organisms is not just the result of the large-scale dysfunction and failure of organ systems and tissues. The cells that make up our tissues undergo ageing, suffering a loss of function in their own ‘organ systems’ and an increasing vulnerability to damage, eventually leading to death or senescence (a state in which a cell is no longer able to replicate).
Every cell in the body is constantly exposed to unavoidable sources of damage, such as radiation from space and chemicals produced by the cell’s own metabolism. These damage the cell’s DNA, proteins, and organs (organelles), and change how the DNA is packaged and read (epigenetics). These changes progressively reduce the ability of the cell to perform its function within the body. Further damage to the DNA is incurred each time a cell divides because of copying errors when the DNA is replicated, and any pre-existing damage is passed on to the daughter cells. Each cellular division also shortens the cell’s telomeres, which cap the ends of the chromosomes and are necessary to protect them from damage.
As we age, our cells themselves become less capable of fulfilling their functions. They become less able to build and manage the proteins that they need (proteostasis), less efficient at producing energy, and less resistant to damage. Furthermore, if sufficient damage is sustained, a cell will either self destruct in a process called apoptosis, or will become senescent and subsequently be destroyed by the immune system. Both of these outcomes are beneficial for an organism in the short term, as damaged cells with the ability to divide risk becoming cancerous. However, as more and more cells succumb to cellular ageing, these processes become detrimental. Large numbers of cells may be lost to apoptosis, while senescent cells accumulate faster than they can be removed. Under these circumstances, senescent cells become harmful due to the signals that they release, which promote a range of age-related diseases including cancer – the very disease that senescence initially serves to prevent.
Principles of the Molecular and Cellular Mechanisms of Aging: https://doi.org/10.1016/j.jid.2020.11.018
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