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What is apoptosis? Apoptosis is the most common form of programmed cell death. It can be triggered via various physical, chemical, and biological factors, and its cellular response is tightly regulated.
The controlled degradation of cellular components that occurs during apoptosis is regulated by caspases, which are a family of proteases activated during apoptosis more details here: Caspase family.
In healthy cells, caspases exist as proenzymes in their inactive forms. Apoptotic signaling activates a caspase cascade caspase -2,-8, -9, and , called initiator caspases. Next, the initiator caspases in turn cleave and activate downstream effector caspases caspase -3, -6, and Effector caspases execute apoptosis by cleaving targeted cellular proteins. Stimuli initiating apoptosis can be internal e.
There are two main receptor types for externally induced apoptosis. Death receptors e. This prompts their activation and assembly into complexes, leading to the activation of intracellular caspases. The other apoptotic receptors are called dependence receptors e. In physiological conditions, they respond to trophic factors and act as an anti-apoptotic stimulus.
However, when their ligand falls below a certain level in the extracellular space, ligand-free receptors trigger the apoptotic response. BAK is a transmembrane protein of the outer mitochondrial membrane. Upon apoptosis induction, BAX undergoes conformational change. This exposes its transmembrane domain, leading to the insertion of BAX into the outer mitochondrial membrane. Apoptosis is reflected in significant cell morphological changes Table 1.
In the earlier phases, a cell undergoing apoptosis loses cell contacts and changes shape. Chromatin condenses in the nucleus and moves toward the nuclear envelope. Condensation of the nucleus pyknosis initiates DNA degradation.
Loss of water results in significant cell shrinkage and blebbing of the plasma membrane with little or no morphological changes to the other cellular organelles. Phosphatidylserine, a lipid present only in the inner layer of the plasma membrane, is now also visible in the outer layer.
Nucleus and cytoplasm fragment into apoptotic bodies. Released cellular proteases lead to disintegration of the cellular skeleton, membranes, and proteins. Neighboring macrophages recognize, engulf, and digest apoptotic bodies, completing the process. What is necrosis? Necrosis is a form of cell injury defined as unregulated cell death resulting from internal or external stresses such as mechanistic injuries, chemical agents, or pathogens.
The process is usually rapid and leads to cell swelling oncosis and bursting due to loss of osmotic pressure Table 1. During necrosis, the loss of plasma membrane integrity induces cellular contents to escape to the extracellular space, causing inflammatory responses.
Cell disintegration is preceded by a series of morphological changes, including disruption of cell organelles, such as swelling of the ER and mitochondria, or decay of the Golgi apparatus.
An influx of calcium ions from the extracellular matrix activates intracellular nucleases that fragment DNA. A small fraction of tertiary stage infections will evolve into gummatous syphilis. Gummatous syphilis is characterized by the formation of chronic gummas, which are soft, tumor-like balls of inflammation granuloma around a necrotic center [12].
These central regions begin to die through coagulative necrosis, as they retain some of the structural characteristics of previously normal tissues.
In contrast, in the granulomas of tuberculosis caused by the bacterium Mycobacterium tuberculosis preexisting structures are obliterated by a form of cell death known as caseous necrosis. Dead cells from caseous necrosis disintegrate but are not completely digested, leaving granular particles. Gummas are most commonly found in the liver gumma hepatis , but can also be found in brain, heart, skin, bone, testis, and other tissues, leading to a variety of potential problems including neurological disorders or heart valve disease [12].
Liquefactive necrosis or colliquative necrosis , in contrast to coagulative necrosis see ischemia , is characterized by the digestion of dead cells to form a viscous liquid mass. This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response.
The necrotic liquid mass is frequently creamy yellow due to the presence of dead leukocytes and is commonly known as pus. Toxins and venoms In the United States, only spider bites from the Brown Recluse spider genus Loxosceles routinely progress to necrosis. In other countries, spiders of the same genus, such as the Chilean Recluse in South America, have the potential to cause necrosis around the area of the spider bite. Toxins such as snake venoms may inhibit enzymes leading to necrotic cell death.
Necrotic wounds have also resulted from the stings of Vespa mandarinia. High doses of paracetamol have been reported to cause hepatocellular necrosis [5]. Physical trauma Tissue damage incurred by physical force can directly lead to cellular breakdown and to loss of blood supply leading to necrosis [15, 16].
This is in addition to necrosis by ischemia and infection that may develop later because of the trauma. Thermal damage Elongated exposure to freezing conditions may cause ice crystals to form in the tissues starting with the skin at nose, finger tips and toes , which causes damage at the cellular level, leading to necrosis.
A burn is a type of injury caused by heat, cold, electricity, chemicals, friction, or radiation. Burns that affect only the superficial skin layers are known as superficial or first-degree burns. In a full-thickness or third-degree burn, the injury extends to all layers of the skin. A fourth-degree burn additionally involves injury to deeper tissues, such as muscle, tendons, or bone. Up to second degree burns form blisters that will ultimately heal on their own. Fat necrosis Fat necrosis is a benign non-suppurative inflammatory process of adipose tissue which was initially described in the breast, presenting itself as a subcutaneous hard lump resembling cancer [17].
In fat necrosis, the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps that will disintegrate membranes. Fat necrosis is associated with trauma of the pancreas or with acute pancreatitis [18], but it can also occur in the salivary glands and in neonates after a traumatic delivery. Immune-mediated vascular damage Fibrinoid necrosis is observed when there are immune complex deposition events occurring within the blood vessel walls.
This action leads to activation of the complement cascade and the subsequent chemotactic influx of neutrophil and monocytic cells associated with a classic Type III hypersensitivity reaction. If necrotic cells and cellular debris are not promptly destroyed and reabsorbed, they tend to attract calcium salts and other minerals and to become calcified. In small vessel vasculitis, fibrin plugs frequently occur in the vessel lumen, but the term fibrinoid usually refers to material outside the lumen of a vessel.
Secondary necrosis Necrosis also occurs when apoptosis happens at such scale that phagocytosis of the apoptotic bodies can no longer keep up, or when phagocytosis for other reasons is not available, thus resulting in lysis of apoptotic cells. Then the necrosis is considered secondary to apoptosis, although the argument is made that secondary necrosis is a natural finish of the apoptotic process [19].
It is important to note that in many pathologies, necrosis and apoptosis happen side-by-side while it is not always clear which was first [1, 6]. There is still a lot to be discovered with respect to the roles that apoptosis, necrosis, and necroptosis play in the genesis of neurodegenerative, cardiovascular, and cancer.
There is still a lot to be discovered with respect to the roles that apoptosis, necrosis, and necroptosis play in the genesis of neurodegenerative, cardiovascular, and cancer References Proskuryakov, S. Konoplyannikov, and V. Gabai, Necrosis: a specific form of programmed cell death?
Exp Cell Res, Rock, K. This lack of energy causes the cell organelles, which are different structures that perform vital functions in the cell, to become disorganized. Likewise, the cytoplasm, which is the part of the interior of the cells where the different organelles are located, breaks down. Some of the alterations that necrosis produces in cell organelles are:.
During necrosis, the DNA splits into random, irregular fragments. This process causes the cells of the immune system to move to the area where the necrosis has occurred, triggering an inflammatory process. This cell death process can occur naturally or as the result of an illness, but without ATP loss. This is because, for apoptosis to take place, it needs to consume energy. A genetically and synthetically motivated command initiates a series of biochemical reactions that lead to changes in cell morphology and, ultimately, to cell death.
All of this is a response to physiological or pathological events. Histologically, it involves the condensation or shrinkage of the cell organelles found in the cytoplasm. Rather, neighboring cells capture it. This process occurs in isolated cells and not in whole areas of tissue. Discover: Cerebral Hypoxia: Types and Causes. In conclusion, apoptosis and necrosis differ in the stimulus that triggers both processes.
There are also differences in the energy requirement, histology, and DNA breakdown. In both processes, cell organelles and the cell membrane are altered.
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