- "Apoptosis is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast."
Process of programmed cell death, which plays a critical role in shaping and sculpting tissues during development.
Introduction to apoptosis: The concept of apoptosis, its importance in cellular processes, and its relation to development.
Molecular mechanisms of apoptosis: The various pathways involved in inducing apoptosis, including the extrinsic and intrinsic pathways.
Caspases: The role of caspases, a family of proteases, in executing the apoptotic process.
Bcl-2 family: The role of the Bcl-2 family of proteins in regulating apoptosis, including their anti- and pro-apoptotic functions.
Mitochondrial regulation of apoptosis: The involvement of mitochondria in the intrinsic pathway of apoptosis, including the release of cytochrome c.
Death receptors: The role of death receptors, such as Fas and TNFR, in the extrinsic pathway of apoptosis.
Inflammation and apoptosis: The relationship between inflammatory processes and apoptosis, including the role of cytokines in regulating apoptosis.
Developmental apoptosis: The importance of apoptosis in shaping tissues, organs, and organisms during development.
Apoptosis in disease: The role of apoptosis in various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.
Therapeutic targeting of apoptosis: The potential for targeting apoptotic pathways as a therapeutic approach to treating various diseases.
Caspase-dependent apoptosis: This type of apoptosis is characterized by the activation of caspase enzymes, which play a central role in the process. Caspase-dependent apoptosis is triggered by various cellular signals, including DNA damage, protein misfolding, and viral infections.
Mitochondrial apoptosis: Mitochondrial apoptosis is initiated from signals that disrupt the mitochondrial outer membrane, leading to the release of pro-apoptotic factors into the cytosol. This can be caused by a variety of stresses, such as oxidative damage, DNA damage, and nutrient deprivation.
ER-stress-induced apoptosis: This type of apoptosis occurs in response to excessive stress on the endoplasmic reticulum (ER), which is responsible for protein synthesis and folding. ER-stress-induced apoptosis is triggered by three signaling pathways: the PERK pathway, the IRE1 pathway, and the ATF6 pathway.
Autophagy-induced apoptosis: Autophagy is a cellular process that degrades damaged organelles and misfolded proteins. In some cases, autophagy can lead to apoptosis when the cellular damage is too severe to be repaired.
T-cell-induced apoptosis: T-cell-induced apoptosis is a form of apoptosis that is mediated by T-lymphocytes. This process is important in the immune response against infections and cancer, and it helps to remove damaged or infected cells.
Death receptor-induced apoptosis: Death receptor-induced apoptosis is mediated by death receptors on the cell surface, which trigger a signaling cascade that leads to apoptosis. This process is triggered by various ligands, such as TNF-alpha and Fas ligand.
Necroptosis: Necroptosis is a form of programmed cell death that is distinct from apoptosis. It is triggered by the activation of death receptors, but it involves a different set of signaling pathways that lead to necrotic cell death.
- "These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation, and mRNA decay."
- "The average adult human loses between 50 and 70 billion cells each day due to apoptosis."
- "For an average human child between eight and fourteen years old, each day the approximate lost is 20 to 30 billion cells."
- "In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis is a highly regulated and controlled process."
- "Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them."
- "Apoptosis can be initiated through one of two pathways. In the intrinsic pathway, the cell kills itself because it senses cell stress, while in the extrinsic pathway, the cell kills itself because of signals from other cells."
- "Both pathways induce cell death by activating caspases, which are proteases, or enzymes that degrade proteins."
- "The two pathways both activate initiator caspases, which then activate executioner caspases, which then kill the cell by degrading proteins indiscriminately."
- "Defective apoptotic processes have been implicated in a wide variety of diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer."
- "Some factors like Fas receptors and caspases promote apoptosis."
- "Some members of the Bcl-2 family of proteins inhibit apoptosis."
- "For example, the separation of fingers and toes in a developing human embryo occurs because cells between the digits undergo apoptosis."
- "Because apoptosis cannot stop once it has begun, it is a highly regulated process."
- "Weak external signals may also activate the intrinsic pathway of apoptosis."
- "Biochemical events lead to characteristic cell changes (morphology) and death."
- "Phagocytes are able to engulf and remove apoptotic bodies before the contents of the cell can spill out onto surrounding cells and cause damage to them."
- "These changes include... DNA fragmentation."
- "Apoptosis is a highly regulated and controlled process that confers advantages during an organism's life cycle."
- "Because apoptosis cannot stop once it has begun, it is a highly regulated process."