Please enable JavaScript.
Coggle requires JavaScript to display documents.
Mitochondria (ROS (funtions (cytochrome c in cytosol (apoptosis),…
Mitochondria
ROS
In complex 1 and 3 superoxide is formed
dismutated in H2O2 by superoxide dismutase (SOD2 or SOD1)
cell death
mitohormesis
ROS in low concentration
protects cell
increase life span
funtions
impair ATP synthesis ATP
cytochrome c in cytosol
apoptosis
induction mitochondrial permeability transition pore (PTP)
membrane permeable to small molecules
redox function
blocked by antioxidants
Mitochondrial dysfunction
more electron leakage
less ATP
decrease mitochondrial membrane potential
more ROS production
more mitochondrial deterioration
mitophagy
inflammation
Maintenance
increase number mitochondria
genes in nuclear genome
proteins transporten via TIM and TOM
increase in size mitochondria
in response to environmental stimuli
aerobic exercise
endurance training
Mitochondrial genome
encodes parts of electron transport chain
encodes rRNA and tRNA
structure
inner membrane
matrix
enzymes for cellular respiration
energy
citric acid cycle
NADH+, FADH2
oxidative phosphorylation
SOD2
cristae
outer membrane
proteins through which moleculas can pass
intermembrane space
SOD1
Loss of proteastasis
unfolded, misfolded, aggregated proteins
age-related pathologies
mechanism that stabilize and correctly folds proteins
HSP family
expressed during stress situations
regulation chaperones
aggregation misfolded proteins
refolded and released
proteolytic system
microautophagy
direct engulfment of cytoplasmic material in lysosome
macroautophagy
phagophore enguls material en form a double membrane around organelle marked for destruction
fusion with lysosome
chaperone mitigated autophagy
protein needs recognition site for hsc70 complex
binds to chaperone
complex binds to lysosomal membrane bound CMA receptor
CMA-substrate/chaperone complex
in lysosome
ubiquitin-proteosome system (UPS)
clearing of unfolded proteins
genomic instability
due to genetic damage throughout life
exogenous threats
endogenous threats
mutations
repair mechanisms
nutrition: calorie restriction
insuline/IGF-1
FoxO
mTOR