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Senescence
Regardless of outside factors, most cells have a built-in "expiration date" at which point the cell can no longer divide. This point is called senescence. Senescent cells may persist for some time but eventually die because they cannot maintain their cellular functions due to the progressive destruction of the telomeres at the ends of the chromosomes. As the human body ages, a greater proportion of our cells become senescent and we can no longer respond to the stressors of everyday life as well. Eventually, senescent cells succumb to forms of programmed death such as apoptosis or phagocytosis.
Apoptosis
This is a form of programmed cell death that is a crucial aspect of development and everyday life. Damaged or unneeded cells dissolve themselves from the inside out, packaging and digesting genetic and protein components for use by other healthy cells. The default state of human cells is one of programmed death, but this state is stopped by the constitutive expression of apoptosis inhibitors. Apoptosis is triggered by a complex biochemical cascade that results in the destruction of these inhibitors.
Apoptosis is a normal function of development. For instance, the hands and feet start out as paddle-like structures in utero and develop distinct fingers and toes when the tissue between the newly formed bones begins to degrade via apoptosis. It can also be induced by various stress and cell death signals from surrounding tissues.
Macrophagy
This is a mechanism of cell death that often works in conjunction with apoptosis. The blood and brain both contain populations of cells called macrophages that are capable of enveloping and devouring other cells in a process called phagocytosis. This process combats infectious bacteria and parasites, as well as inflamed, injured or infected cells marked for death via antibodies or cell death factors. One such factor is phosphatidylserine, a molecule that acts as a marker for cells undergoing apoptosis when it is expressed at the outside of the cell.
Many autoimmune diseases are caused by inappropriate phagocytosis. For instance, type 1 diabetes is caused by the phagocytosis of insulin-producing beta-cells in the pancreas.
Necrosis
Not all forms of cell death are programmed. Severe cell trauma caused by physical, chemical or temperature damage results in necrosis. Unlike apoptosis, which packages the cell contents for recycling, necrotic cells simply die and release their contents into the outside medium. Some of these contents, such as lysosome enzymes (the cell's digestive system), are harmful to surrounding cells and can trigger a cascade of cell death. Gangrene is a medical condition triggered by runaway tissue necrosis.
Viral Infections
Viruses are small DNA- or RNA-based pathogens that have no cells of their own. In order to reproduce, viruses inject their genetic material into host cells and take over the cellular machinery to produce new copies of the virus. These viruses often inhibit apoptosis so the infected cell cannot kill itself. Instead, the virus particles replicate and build up inside the cell until it bursts open, releasing the virus into the outside medium, where the myriad copies can infect more cells.