Acetylation in Mitochondria Dynamics and Neurodegeneration

Waddell, Jaylyn; Banerjee, Aditi; Kristián, Tibor

doi:10.3390/cells10113031

Cited by 10 publications

(9 citation statements)

References 180 publications

(246 reference statements)

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“…[10][11][12] In addition to changing the expression of MnSOD, alterations of MnSOD activity, by modulating protein level acetylation status of this mitochondrial isoform, is considered as an evolving concept in understanding ROS led pathogenesis of neurodegenerative brain disorders. 13 Sirtuin3 (SIRT3), a mitochondrial isoform of SIRTUINs family deacetylase, is now emerging as a master regulator of the mitochondrial functions. 13,14 This does so mainly by deacetylating a number of mitochondrial proteins amongst which MnSOD is known to be the most important one.…”

mentioning

confidence: 99%

“…13 Sirtuin3 (SIRT3), a mitochondrial isoform of SIRTUINs family deacetylase, is now emerging as a master regulator of the mitochondrial functions. 13,14 This does so mainly by deacetylating a number of mitochondrial proteins amongst which MnSOD is known to be the most important one. 14 There are some reports on enhanced MnSOD activity due to its deacetylation by SIRT3.…”

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confidence: 99%

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Hippocampus mitochondrial MnSOD activation by a SIRT3 activator, honokiol, correlates with its deacetylation and upregulation of FoxO3a and PGC1α in a rat model of ammonia neurotoxicity

Anamika

Roy

Trigun

2023

J of Cellular Biochemistry

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We have recently reported that honokiol (HKL), by activating mitochondrial SIRT3, normalizes reactive oxygen species level and mitochondrial integrity in hippocampus of the moderate grade hepatic encephalopathy (MoHE) rat model of ammonia neurotoxicity. To delineate the mechanism by which HKL does so, the present study describes activity versus level of the deacetylated mitochondrial Mn‐superoxide dismutase (MnSOD) and expression of MnSOD versus levels of its main transcription regulators, FoxO3a and PGC1α, in the hippocampus of the MoHE rats. MoHE in rat was developed by administration of 100 mg/kg bw thioacetamide i.p. for 10 days. The study parameters were compared between the control, the MoHE rats and the MoHE rats treated with HKL (10 mg/Kg b.w.) for 7 days. As compared to control, the hippocampus mitochondria from MoHE rats showed a significantly declined activity of MnSOD vs enhanced lipid peroxidation coinciding with the increased level of its acetylated form. The HKL treatment could, however, normalize all these parameters in those MoHE rats. Also, a significantly reduced expression of MnSOD in the hippocampus of the MoHE rats coincided with a similar decline in transcript level of Foxo3a and Pgc1α. This was consistent with the reduced level of immuno‐stained Foxo3a and Pgc1α proteins in hippocampus DG, CA1 and CA3 regions of those MoHE rats. However, all these factors were observed to be restored back to their normal levels due to the treatment with HKL. As HKL is a specific activator of mitochondrial SIRT3, these findings suggest involvement of Sirt3 activation led deacetylation of MnSOD and upregulation of its transcription activators, FoxO3a and PGC1α, in restoring mitochondrial MnSOD level in the hippocampus of the MoHE rat model of ammonia neurotoxicity.

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confidence: 99%

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confidence: 99%

Hippocampus mitochondrial MnSOD activation by a SIRT3 activator, honokiol, correlates with its deacetylation and upregulation of FoxO3a and PGC1α in a rat model of ammonia neurotoxicity

Anamika

Roy

Trigun

2023

J of Cellular Biochemistry

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“…In addition, cytoskeleton reorganization and mitochondrial metabolism provoked by mechanical stimulation may be mediated by epigenetic reprogramming and post-translational modification. Cytoskeletal post-translational modification contributes to mitochondrial dynamics [ 174 ], VSMC mobility and AS progression [ 175 , 176 ]. Vascular stiffness and shear stress can induce epigenetic regulation in VSMCs such as DNMT1 and miRNA level [ 177 , 178 ].…”

Section: Conclusion and Discussionmentioning

confidence: 99%

Mitochondria spatially and temporally modulate VSMC phenotypes via interacting with cytoskeleton in cardiovascular diseases

Song

et al. 2023

Redox Biology

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“…Additionally, it is not known whether SLC25A51 activity can be modulated by post-translational modifications, particularly acetylation. Mitochondrial deacetylase Sirtuin 3 (SIRT3) is NAD +dependent and deacetylates several enzymes of the Krebs cycle, respiratory chain, and the ATP synthase (Waddell et al, 2021).…”

Section: Intracellular Compartmentation and Transport Of Nad +mentioning

confidence: 99%

Brain energy metabolism: A roadmap for future research

Rae,

Baur,

Borges

et al. 2024

Journal of Neurochemistry

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Although we have learned much about how the brain fuels its functions over the last decades, there remains much still to discover in an organ that is so complex. This article lays out major gaps in our knowledge of interrelationships between brain metabolism and brain function, including biochemical, cellular, and subcellular aspects of functional metabolism and its imaging in adult brain, as well as during development, aging, and disease. The focus is on unknowns in metabolism of major brain substrates and associated transporters, the roles of insulin and of lipid droplets, the emerging role of metabolism in microglia, mysteries about the major brain cofactor and signaling molecule NAD+, as well as unsolved problems underlying brain metabolism in pathologies such as traumatic brain injury, epilepsy, and metabolic downregulation during hibernation. It describes our current level of understanding of these facets of brain energy metabolism as well as a roadmap for future research.

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Acetylation in Mitochondria Dynamics and Neurodegeneration

Cited by 10 publications

References 180 publications

Hippocampus mitochondrial MnSOD activation by a SIRT3 activator, honokiol, correlates with its deacetylation and upregulation of FoxO3a and PGC1α in a rat model of ammonia neurotoxicity

Hippocampus mitochondrial MnSOD activation by a SIRT3 activator, honokiol, correlates with its deacetylation and upregulation of FoxO3a and PGC1α in a rat model of ammonia neurotoxicity

Mitochondria spatially and temporally modulate VSMC phenotypes via interacting with cytoskeleton in cardiovascular diseases

Brain energy metabolism: A roadmap for future research

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