Apoptosis pathway is cell signal which leads to programmed cell death.
Everyday few billion cells in the human body get deleted by it.
But the function of this pathway is beneficial to our body as it removes harmful or defective cells.
When an injury damages a cell in the body, first there is an effort for repair mechanism.
If the repair mechanism is not fruitful, it goes for cell death pathway to remove the cell.
This slow death pathway is called as apoptosis and it enhances the lifespan of the person.
Failure of this apoptosis pathway can lead to the development of diseases like cancer generation in the human body.
Cancer cells in the human body do not have this mechanism of cell death. Hence, they grow unhindered leading to degeneration of body and life.
Apoptosis pathway
This pathway is controlled by 3 important pathways like
1. The intrinsic pathway
2. Extrinsic pathway and
3. Granzyme pathway (perforin).
All these pathways are carried by enzymes like caspases and proteins like Bcl, cytochrome-C, etc.
Intrinsic pathway: This is triggered by toxins, radiation, oxidative stress or even lack of oxygen. It leads to mitochondrial damage———————> activation of caspase-9———>Activation of caspase-3 then cell death.
Mitochondria disruption is key is intrinsic pathway as it releases cytochrome-C which activate caspase-9
Extrinsic pathway: Here a death ligand binds to death receptor and activates caspase-8————-> activation of caspase-3.
Granzyme based
This is immune-based reaction wherein cytotoxic -T cells lead to the release of granzyme which activates caspase-3 and caspase-10.
So, in all these three methods, caspase-3 is activated which activates endonucleases leading to degradation of chromosomal DNA and also damage of nuclear and cytoskeletal proteins.
Then there is cytoplasmic condensation and nuclear fragmentation leading to the formation of apoptotic bodies.
There are many enzymes and proteins which are directly or indirectly involved in the apoptosis pathway which are beyond the scope of this simple presentation.