Apoptosis is a highly regulated process of programmed cell death that occurs in multicellular organisms. It is characterized by a series of distinct morphological changes, including cell shrinkage, nuclear fragmentation, and the formation of apoptotic bodies. These changes are triggered by a cascade of molecular events, ultimately leading to the dismantling of the cell without causing inflammation.
There are two primary pathways involved in apoptosis:
1. Extrinsic or Death Receptor Pathway:
- This pathway is triggered by external signals, often from neighboring cells.
- It involves the activation of death receptors, transmembrane proteins that bind to specific ligands.
- Upon ligand binding, death receptors recruit adaptor proteins, which in turn activate caspase-8.
- Caspase-8 is a key executioner caspase that initiates the downstream apoptotic cascade.
2. Intrinsic or Mitochondrial Pathway:
- This pathway is triggered by intracellular stresses, such as DNA damage, hypoxia, or oxidative stress.
- It involves the release of cytochrome c from the mitochondria into the cytoplasm.
- Cytochrome c activates caspase-9, another executioner caspase.
- Caspase-9 then activates caspase-3, which ultimately leads to the breakdown of cellular components.
Both pathways converge on the activation of executioner caspases, which cleave various cellular proteins, ultimately leading to the dismantling of the cell.
Examples of apoptosis in action:
- During development, apoptosis removes unnecessary cells and shapes organs.
- In the immune system, apoptosis eliminates infected cells and self-reactive lymphocytes.
- In response to tissue injury, apoptosis removes damaged cells.
Apoptosis is essential for maintaining tissue homeostasis and preventing uncontrolled cell growth.
