What is apoptosis and why is it beneficial for cells to clean themselves up?
Apoptosis is an indispensable clean-up mechanism that keeps your body healthy, but balance is everything: too little increases the risk of cancer, too much damages the brain and other vulnerable tissue.
Every day, billions of cells in your body die in an orderly, quiet way. This is called apoptosis: a built-in self-destruction programme that the body uses to remove damaged, aged or redundant cells. The cell shrinks, breaks down neatly, and is cleared away by surrounding cells. No inflammation is involved.
That is precisely the difference from unwanted cell death, such as during a heart attack. In that case a cell swells and bursts open, which does trigger a substantial inflammatory response and causes additional tissue damage. Apoptosis is the tidy alternative: everything is handled without making a mess.
Apoptosis is essential at two moments. During the formation of the body, redundant cells are cut away through apoptosis, quite literally the way the skin between your fingers disappears. After birth, the mechanism keeps tissue healthy by replacing aged or damaged cells. Apoptosis also helps during infections: by allowing infected cells to die off before a virus or bacterium can spread further, the body limits the damage.
The balance is critical, however. Too little apoptosis and cells that should really be removed keep dividing, which can contribute to cancer. Too much apoptosis and the body clears away its own still-healthy cells. The latter plays a role in brain diseases such as Alzheimer's and after a stroke: adult nerve cells can barely renew themselves, so every neuron that is needlessly lost is a permanent loss.
Apoptosis is also not the only form of programmed cell death. Variants exist that do trigger inflammation, and these play a role in serious infections such as sepsis. The interplay between these different pathways makes targeted intervention difficult. Existing and future research is focused on restoring the balance, but concrete treatments are not yet widely available.
Based on strong mechanistic and clinical literature (PMID 38242081, 7856735, 29488822, 40817040). The basic biology of apoptosis is well established; its role in sepsis and therapeutic applications are less mature.
Why do cells lose their ability to repair themselves over time?
Cells lose their repair capacity through a combination of declining energy stores, impaired DNA repair and the accumulation of 'burned-out' cells that secrete inflammatory substances. These are well-supported mechanisms, although it is still too early to act on them through supplements or therapies.
Can DNA damage in your cells repair itself?
Your cells repair DNA damage continuously and systematically, but the system is not infallible: chronic overload or a defect in the repair pathways increases the risk of cancer and age-related diseases.
What are free radicals and what do they do to your cells?
Free radicals are unavoidable by-products of your metabolism that are useful in small amounts but, in excess, damage DNA, proteins and cell membranes. Antioxidant supplements offer little practical benefit; the best protection lies in avoiding external sources such as smoking, fine particulate matter and excessive UV exposure.
What is the role of inflammation in cellular ageing?
Inflammation and cellular senescence reinforce each other in two vicious cycles, leading to tissue damage and age-related diseases. Both protecting your cells against oxidative damage (think sun protection and lifestyle) and future targeted therapies aim to break this cycle.
How does air pollution damage your cells from the inside?
Air pollution damages your cells from the inside through oxidative stress: fine particulate matter causes an excess of harmful oxygen molecules that attack your DNA, energy factories, and immune system. Protection begins with limiting exposure, because the damage occurs at the cellular level.
Why do some cells stop dividing as you age?
Cells stop dividing as a protection against damage and cancer, but the accumulation of such stopped cells contributes over the years to inflammation and age-related diseases. Drugs that target this are promising in animal research, but are not yet ready for use outside clinical studies.