nemoci-sympt/METABOLISMUS/mitochondrie/metabolizmus/autofagocytoza
Mitophagy
- Engulfed within a double-membrane vacuole called the autophagosome
- Eventually gets fused with lysosomes to form the autolysosome
- Complete digestion [9]
- Specific receptors on the surface of the organelles
- Targeting them to the pre-autophagosome [9]
- Anabolic conditions
- High glucose and amino acid availability
- Activate mammalian target of rapamycin complex 1 (mTORC1)
- Inhibits autophagy
- Cyclic AMP (cAMP) levels are increased
- Increased inositol-1,4,5-trisphosphate (Ins(1,4,5)P3)
- Release of Ca2 + from the ER
- Inhibition of autophagy via Ca2 +-activated calpains [9]
- Catabolic conditions
- Activate AMPK cascade
- Basic helix–loop–helix leucine zipper transcription factor EB (TFEB)
- Trigger autophagy [9]
- Low energy (e.g. starvation)
- TFEB is phosphorylated
- Migrates to the nucleus
- Promotes autophagic and lysosome biogenetic programs [9]
- AMPK
- Inhibits mTORC1
- Activates UNC51-like kinase 1 (ULK1) complex
- Activates serine/threonine protein kinase
- Stimulates the autophagic cascade [9]
- Chronic treatment with rapamycin
- Activates autophagy
- Significantly delayed
- Disease progression and fatal outcome of a Ndufs4-/-mouse
- Lacks the 18 kDa Ndufs4 subunit of complex I [9]
Mitophagy
- Engulfed within a double-membrane vacuole called the autophagosome
- Eventually gets fused with lysosomes to form the autolysosome
- Complete digestion [9]
- Specific receptors on the surface of the organelles
- Targeting them to the pre-autophagosome [9]
- Anabolic conditions
- High glucose and amino acid availability
- Activate mammalian target of rapamycin complex 1 (mTORC1)
- Inhibits autophagy
- Cyclic AMP (cAMP) levels are increased
- Increased inositol-1,4,5-trisphosphate (Ins(1,4,5)P3)
- Release of Ca2 + from the ER
- Inhibition of autophagy via Ca2 +-activated calpains [9]
- Catabolic conditions
- Activate AMPK cascade
- Basic helix–loop–helix leucine zipper transcription factor EB (TFEB)
- Trigger autophagy [9]
- Low energy (e.g. starvation)
- TFEB is phosphorylated
- Migrates to the nucleus
- Promotes autophagic and lysosome biogenetic programs [9]
- AMPK
- Inhibits mTORC1
- Activates UNC51-like kinase 1 (ULK1) complex
- Activates serine/threonine protein kinase
- Stimulates the autophagic cascade [9]
- Chronic treatment with rapamycin
- Activates autophagy
- Significantly delayed
- Disease progression and fatal outcome of a Ndufs4-/-mouse
- Lacks the 18 kDa Ndufs4 subunit of complex I [9]
