Cell death

Dead cell, according to Nomenclature Committee on Cell Death (NCCD), is the cell that displays any one of the properties that are listed below:

• Disappearance of plasma membrane integrity, in vivo.
• Complete fragmentation of nucleus and other components of cell into separate partition.
• Engulfment of these partitions by adjacent cell, in vivo ^[1].

Two major classes of cell death in terms of their functional aspects named Programmed and non-Programmed cell death ^[2]. While programmed cell death (PCD) occurs in an organized manner via intracellular processes, non- PCD, attributed to necrosis, has unorganized style. Non- PCD generally sourced from acute injury and infection. In general, PCD is observed in biological development operations, cancer therapies and cancer propagation^[3].

Apoptosis is one of the type of cell death which have signal transduction path as seen in Figure 2.

As last step of apoptosis cell is divided to minor parts named apoptotic bodies. These bodies are cleared by phagocytes and then processed via the help of lysosomal enzymes. By this way, release of particles that may cause inflammation is prevented ^[4].

Autophagy provides degradation by the help of autophagic vacuoles ^[5]. The process start with collection of cytoplasmic elements into autophagosomes, a double membraned compartment. After that these compartments combine with lysosome. Via this event degradation of collected materials is aimed and achieved ^[6] Cell exposing to autophagy can be processed by neighboring cells, by phagocytosis^[7][8].

Apoptosis and autophagy were known as sole styles of PCD before programmed necrosis emerges. Programmed necrosis includes subtypes, necroptosis, pyroptosis, partonatos and ferroptosis ^[9]. These newly discovered subtypes may provide solution for cancers that has ability to escape from apoptosis ^[10]. Among four subtypes of programmed necrosis, necroptosis is the best described one ^[11].

Prevalenly, induction of necroptosis takes place by the help trigger of death receptor. Because this type of PCD shares similarities with both necrosis and apoptosis, necroptosis name is given as a combination of names necrosis and apoptosis. Necroptosis utilizes organized cellular particles, as seen in apoptosis, while result in burst of cell, like diagnosed in necrosis. Burst of the cell causes release of damage- associated molecular patterns (DAMPs)^[12].

Parthonatos is the cell that is triggered via overstimulation of PARP. PARP is a DNA repairing enzyme which means it can be activated by providing genotoxic- stress ^[13].

Pyroptosis uses inflammatory caspases, this condititon makes it highly inflammatory. Pathological agent, cancer and other some physiological issues result in pyroptosis. Initiation of the cell death begins with emergence of active multi- protein coımplex inflammasomes. Presence of Gasdermin D, found in the structure of inflammasomes and behaves as a substrate for inflammatory aspases, is an obligation for pyrotosis ^[14][15]. • Pro-inflammatory programmed cell death different than apoptosis -Involves activation of caspase-1 which cleaves the precursor form of IL-1 to generate biologically active IL-1 (fever inducing cytokine). • Important in the host defense system for fighting microbial pathogens – In monocytes, macrophages, and dendritic cells infected with certain microbes – Microbial pathogens that may be killed by pyroptosis

  -Salmonella typhimurium, Shigella flexneri, Legionella pneumophila, Pseudomonas aeruginosa, Candida albicans, Adenovirus, and Influenza virus

• Also implicated in pathogenesis of – Myocardial infarction (MI), Neurodegenerative diseases, Inflammatory Bowel Disease (IBD), Cerebral Ischemia, and Endotoxic Shock.

Ferroptosis observed in various degenerative diseases. The reason that drives cell to ferroptosis is accumulation lethal ROS in an intracellular iron- dependent manner. Ferroptosis is fairly related with peroxidation of lipids. Lowered level of functioning of glutathione preoxidase 4 (GPX4), a lipid repair enzyme and it is able to prevent ferroptosis, and accumulation of lipid preoxidase provoke ferroptosis. Disrupted outer membrane of mitochondria, increased mitochondrial membrane density and decrease in the overall size of the mitochondria are the signs of ferroptosis^[16][17].

In plants apoptotic bodies cannot found because of presence of cell wall. And another difference in plant cell death is lack of phagocytes in plants. Therefore, it is not true to catagorize death of a plant cell as apoptosis, even regardless of the aspects^[18].

Lytic vacuoles take care of recycling of cell components, as lysosome do this job in animal cells^[19]. These vacuoles play an significant role at a special type of a cell death called vacuolar cell death^[20]. Vacuolar cell death functions via sliding of cytoplasmic content to lytic vacuole and fallowed by dismantlement of slided cytoplasmic elements ^[21]. Mitochondria and other organels remain intact till vacuole membrane is disrupted. While in some cases, high degree degradation of cell wall occurs, as seen in aerenchyma formation, it is not observed in other cases like differentiation of xylem cells of vascuolar plants^[22][23][24].

Some aspects of vacuolar cell death:

• Big lytic vacuoles are generated.
• Nuclear envelope disrupted.
• Vacuolar membrane (tonoplast) is ruptured.

Some aspects of necrosis in plant cells:

• Mitochondria gain water from cytoplasm so it is swelling.
• Plasma membrane is disrupted in early phase of the death process.
• Cell corpse remains mostly unprocessed (because plants are devoid of phagocyte cells).
• Protoplast shrinks however no visual alteration is able to seen at overall structure of the plant cell.

Hyper sensitive response displays aspects that are combination of vacuolar cell death and necrosis^[25].