Lecture 9 - Apoptosis Autophagy and necrosis in comparison Flashcards
Autophagy is the
degradation process of redundant or faulty cell components, mediated by a unique organelle, the autophagosome
Autophagy has been described as
the cell’s major adaptive strategy in response to metabolic challenges
The first “line of defense”
A basal level of autophagic flux is inherent to all eukaryotic cells with a lysosomal system
most long-lived proteins are degraded in lysosomes via the
Autophagic pw
- More than 99% of intracellular proteins are long-lived
This rate of autophagosome production and removal is highly dynamic and controlled
The response to perturbations in the extracellular environment through changing the autophagic flux enables the cell to
be accurately in tune with intracellular metabolic demands
Dynamics between modes of cell death
multiple pathological conditions present themselves with morphological overlap
Effects of autophagy induction on apoptosis
Ischaemia induces autophagy as stress response
Enhanced autophagy protects against simulated ischaemia reperfusion (sI/R) injury
Effects of autophagy induction/inhibition on apoptosis
Increased autophagy (RAPA) delays ischaemia (SI)induced apoptosis onset
Decreased autophagy (3MA) increases SI induced apoptosis
Effects of autophagy induction/inhibition on necrosis
The caspase inhibitor zVAD induces necrosis
Autophagy induction (Rapamycin) protects from zVAD induced necrosis
Autophagy inhibition (Chloroquine) enhances zVAD induced necrosis
Effects of autophagy induction/inhibition on necrosis
Increased autophagy (RAPA) delays ischaemia (SI)induced necrosis
Effects of decreased autophagy on intracellular parameters that affect the induction of apoptosis and necrosis.
Mapping out the 3 major pathways that indicate the cross talk between autophagic protein degradation, apoptotic and necrotic cell death