nemoci-sympt/METABOLISMUS/mitochondrie/metabolizmus/biogeneze
Množení mitochondrií
- Podobným binárnímu dělení bakterií
- Při dělení buňky nedochází k žádné kontrolované segragaci mitochondrií do dceřiných buněk
- MtDNA mezi nové buňky distribuována zcela náhodně
- Dceřiné buňky tak mohou získat zcela různý počet normálních a mutací zatížených mitochondrií
- Homoplazmie
- Buňka obdrží pouze normální mitochondrie
- Pouze mutované mitochondrie
- Heteroplazmie
- Obdrží směs normálních a mutovaných mitochondrií
Množení mitochondrií
- Podobným binárnímu dělení bakterií
- Při dělení buňky nedochází k žádné kontrolované segragaci mitochondrií do dceřiných buněk
- MtDNA mezi nové buňky distribuována zcela náhodně
- Dceřiné buňky tak mohou získat zcela různý počet normálních a mutací zatížených mitochondrií
- Homoplazmie
- Buňka obdrží pouze normální mitochondrie
- Pouze mutované mitochondrie
- Heteroplazmie
- Obdrží směs normálních a mutovaných mitochondrií
Mitochondrial biogenesis
- Occurs by growth and division of pre-existing organelles
- Process via which cells increase their individual mitochondrial mass
- Organelles double their size and divide
- Rise to two identical daughter cells [6]
- Temporally coordinated with cell cycle events
- Not only produced in association with cell division [6]
- mitochondrial biogenesis involves:
- Fusion/fission
- Requires protein import
- Processing and cardiolipin biosynthesis [8]
- Higher mitochondrial copy number (or higher mitochondrial mass) is protective for the cell [7]
Pokud nejsou narušené a neprodukují nadbytek volných radikálů...
- Can be produced in response to an
- Oxidative stimulus
- An increase in the energy requirements of the cells
- To exercise training
- To electrical stimulation
- To hormones
- During development
- In certain mitochondrial diseases, etc. [6]
- Correct mitochondrial biogenesis
- Relies on the spatiotemporally coordinated synthesis and import
- Of 1000 proteins encoded by the nuclear genome [8]
- Treat several diseases through triggering mitochondrial biogenesis
- Advanced mitochondrial therapies to
- Chronic and degenerative diseases
- mitochondrial diseases
- Lifespan extension
- Mitohormesis
- Intracellular signaling [6]
- In mitochondrial diseases
- Mutation in the mitochondrial DNA
- Loss of functionality of the OXPHOS system
- Depletion of ATP
- Overproduction of ROS
- Induce further mtDNA mutations [6]
- Compensatory mechanisms adaptation to the energetic deficits in mitochondrial diseases
- Mitochondria to produce more energy even under mitochondrial defect-conditions
- Overexpression of antioxidant enzymes
- mitochondrial biogenesis
- Overexpression of respiratory complex subunits
- Metabolic shift to glycolysis [6]
- Bezafibrate
- Activate the PPAR-PGC-1? axis [6]
- resveratrol
- Activation of AMPK [6]
- Sirt1 agonists
- Quercetin or resveratrol [6]
- Addition of antioxidant supplements
- Neural differentiation
- Implication of mitochondrial biogenesis on neuronal differentiation
- Timing, its regulation by specific signaling pathways
- New potential therapeutic strategies [6]
- mitochondrial dynamic balance between
- mitochondrial fusion,
- Fission
- Quality control systems
- mitochondrial biogenesis [6]
- Pathways leading to mitochondrial biogenesis
- Implication of different regulators
- AMPK, SIRT1, PGC-1?, NRF1, NRF2, Tfam, etc.
- Specific case of neuronal development [6]
- Ameliorate mitochondrial-based diseases
- Induction of PGC-1alpha via activation of PPAR receptors
- Rosiglitazone
- Bezafibrate [6]
- Modulating its activity by AMPK
- AICAR, metformin, resveratrol [6]
- By SIRT1
- SRT1720 and several isoflavone-derived compounds [6]
- Regulation of estrogen receptors, their implication on
- mitochondrial biogenesis
- mitochondrial function
- ROS production [6]
- Free radicals
- As second messengers
- Triggering signals which induce gene expression [6]
- Can trigger mitochondriogenesis [6]
- Periods of active inflammation
- Mitochondria are frequently damaged by oxidative and nitrosative stress
- Elevated levels of endogenous free radicals trigger
- Mitochondriogenesis
- Mitophagy [6]
- Case of the NO/cGMP/PGC-1? axis
- The CO/HO-1 system
- The HS2/Akt/NRF-1/-2 axis [6]
- Several well known drugs can interact to induce mitochondriogenesis
- Inducing mitochondrial biogenesis and quality control
- Key process on lifespan extension
- Caloric restriction
- Endurance exercise
- Dietary supplementation with
- Mixture of essential amino acids
- Enriched in branched-chain amino acids (BCAAs) [6]
- New pharmacological strategies seem to be very promising
- Small SIRT1 activators (SRT1720, SRT2183, SRT1460)
- Other sirtuin activators such as oxazolo[4,4-b]pyridine and imidazol[1,2-b]thiazole derivatives
- Small GSK-3 inhibitors
- SB216763
- ZLN005 (with unknown action mechanism) [6]
- ENOS activators
- AVE compounds [6]
- Low concentrations of free radicals
- Promoters of mitochondrial biogenesis and lifespan extension
- Concept of mitochondrial hormesis or mitohormesis
- Exposure of a cell or an organism to a low dose of one stressor triggers an adaptive response that protects [6]
- Synonyma
- Autoprotection
- Heteroprotection
- Preconditioning
- Adaptive responses
- Compensatory mechanisms
- Hormesis
- Xenohormesis, etc.
- Diphasic, biphasic, bitonic, bell-shaped, Ushaped, inverted-U-shaped, etc. [6]
- Modest production of free radicals by this organelle can act as second messengers to trigger mitochondriogenesis [6]
- Investigated in skeletal muscle and brown adipose tissue
- Peroxisome proliferator-activated receptor gamma (PPARgamma) coactivators 1alpha and beta (the PGC family)
- PCG-1 alpha interact with and activate several transcription factors, including:
- Nuclear Respiratory Factors (NRF1 and 2)
- Peroxisomal Proliferator Activator receptors (PPAR alpha-gamma)
- NRFs and PPARs in turn increase the transcription of genes related to
- Oxidative phosphorylation (OXPHOS)
- Fatty acid oxidation (FAO) pathways [9]
Mitochondrial biogenesis
- Occurs by growth and division of pre-existing organelles
- Process via which cells increase their individual mitochondrial mass
- Organelles double their size and divide
- Rise to two identical daughter cells [6]
- Temporally coordinated with cell cycle events
- Not only produced in association with cell division [6]
- mitochondrial biogenesis involves:
- Fusion/fission
- Requires protein import
- Processing and cardiolipin biosynthesis [8]
- Higher mitochondrial copy number (or higher mitochondrial mass) is protective for the cell [7]
Pokud nejsou narušené a neprodukují nadbytek volných radikálů...
- Can be produced in response to an
- Oxidative stimulus
- An increase in the energy requirements of the cells
- To exercise training
- To electrical stimulation
- To hormones
- During development
- In certain mitochondrial diseases, etc. [6]
- Correct mitochondrial biogenesis
- Relies on the spatiotemporally coordinated synthesis and import
- Of 1000 proteins encoded by the nuclear genome [8]
- Treat several diseases through triggering mitochondrial biogenesis
- Advanced mitochondrial therapies to
- Chronic and degenerative diseases
- mitochondrial diseases
- Lifespan extension
- Mitohormesis
- Intracellular signaling [6]
- In mitochondrial diseases
- Mutation in the mitochondrial DNA
- Loss of functionality of the OXPHOS system
- Depletion of ATP
- Overproduction of ROS
- Induce further mtDNA mutations [6]
- Compensatory mechanisms adaptation to the energetic deficits in mitochondrial diseases
- Mitochondria to produce more energy even under mitochondrial defect-conditions
- Overexpression of antioxidant enzymes
- mitochondrial biogenesis
- Overexpression of respiratory complex subunits
- Metabolic shift to glycolysis [6]
- Bezafibrate
- Activate the PPAR-PGC-1? axis [6]
- resveratrol
- Activation of AMPK [6]
- Sirt1 agonists
- Quercetin or resveratrol [6]
- Addition of antioxidant supplements
- Neural differentiation
- Implication of mitochondrial biogenesis on neuronal differentiation
- Timing, its regulation by specific signaling pathways
- New potential therapeutic strategies [6]
- mitochondrial dynamic balance between
- mitochondrial fusion,
- Fission
- Quality control systems
- mitochondrial biogenesis [6]
- Pathways leading to mitochondrial biogenesis
- Implication of different regulators
- AMPK, SIRT1, PGC-1?, NRF1, NRF2, Tfam, etc.
- Specific case of neuronal development [6]
- Ameliorate mitochondrial-based diseases
- Induction of PGC-1alpha via activation of PPAR receptors
- Rosiglitazone
- Bezafibrate [6]
- Modulating its activity by AMPK
- AICAR, metformin, resveratrol [6]
- By SIRT1
- SRT1720 and several isoflavone-derived compounds [6]
- Regulation of estrogen receptors, their implication on
- mitochondrial biogenesis
- mitochondrial function
- ROS production [6]
- Free radicals
- As second messengers
- Triggering signals which induce gene expression [6]
- Can trigger mitochondriogenesis [6]
- Periods of active inflammation
- Mitochondria are frequently damaged by oxidative and nitrosative stress
- Elevated levels of endogenous free radicals trigger
- Mitochondriogenesis
- Mitophagy [6]
- Case of the NO/cGMP/PGC-1? axis
- The CO/HO-1 system
- The HS2/Akt/NRF-1/-2 axis [6]
- Several well known drugs can interact to induce mitochondriogenesis
- Inducing mitochondrial biogenesis and quality control
- Key process on lifespan extension
- Caloric restriction
- Endurance exercise
- Dietary supplementation with
- Mixture of essential amino acids
- Enriched in branched-chain amino acids (BCAAs) [6]
- New pharmacological strategies seem to be very promising
- Small SIRT1 activators (SRT1720, SRT2183, SRT1460)
- Other sirtuin activators such as oxazolo[4,4-b]pyridine and imidazol[1,2-b]thiazole derivatives
- Small GSK-3 inhibitors
- SB216763
- ZLN005 (with unknown action mechanism) [6]
- ENOS activators
- AVE compounds [6]
- Low concentrations of free radicals
- Promoters of mitochondrial biogenesis and lifespan extension
- Concept of mitochondrial hormesis or mitohormesis
- Exposure of a cell or an organism to a low dose of one stressor triggers an adaptive response that protects [6]
- Synonyma
- Autoprotection
- Heteroprotection
- Preconditioning
- Adaptive responses
- Compensatory mechanisms
- Hormesis
- Xenohormesis, etc.
- Diphasic, biphasic, bitonic, bell-shaped, Ushaped, inverted-U-shaped, etc. [6]
- Modest production of free radicals by this organelle can act as second messengers to trigger mitochondriogenesis [6]
- Investigated in skeletal muscle and brown adipose tissue
- Peroxisome proliferator-activated receptor gamma (PPARgamma) coactivators 1alpha and beta (the PGC family)
- PCG-1 alpha interact with and activate several transcription factors, including:
- Nuclear Respiratory Factors (NRF1 and 2)
- Peroxisomal Proliferator Activator receptors (PPAR alpha-gamma)
- NRFs and PPARs in turn increase the transcription of genes related to
- Oxidative phosphorylation (OXPHOS)
- Fatty acid oxidation (FAO) pathways [9]
