Internship: A time to prioritise

Anamika, Fnu

doi:10.20529/ijme.2022.071

Cited by 6 publications

(7 citation statements)

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“…Among Sirtuins, SIRT3 is the main mitochondrial deacetylase and plays an important role in the maintenance of mitochondrial homeostasis as a stress response protein. SIRT3 increases FOXO3A DNA-binding activity as well as FOXO3A-dependent gene expression [29], which leads to increased respiration to sustain energy metabolism, transactivates SOD and other antioxidant enzymes [30], and activates the transcription of mitophagy genes [24,31,32]. Our results revealed a significant decline of FOXO3A protein expression with the aging of APOE4 mice, implying an influence on mitochondrial oxidative stress in these mice.…”

Section: Discussionmentioning

confidence: 54%

The Dynamic SUMOylation Changes and Their Potential Role in the Senescence of APOE4 Mice

Xu,

Cai,

Sang

et al. 2023

Biomedicines

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The ε4 allele of apolipoprotein E (APOE4) and aging are the major risk factors for Alzheimer’s disease (AD). SUMOylation is intimately linked to the development of AD and the aging process. However, the SUMOylation status in APOE4 mice has not been uncovered. In this study, we investigated SENP1 and SUMOylation changes in the brains of aged APOE3 and APOE4 mice, aiming to understand their potential impact on mitochondrial metabolism and their contribution to cellular senescence in APOE4 mice. Concurrently, SUMO1-conjugated protein levels decreased, while SUMO2/3-conjugated protein levels increased relatively with the aging of APOE4 mice. This suggests that the equilibrium between the SUMOylation and deSUMOylation processes may be associated with senescence and longevity. Our findings highlight the significant roles of SENP1 and SUMOylation changes in APOE4-driven pathology and the aging process.

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Section: Discussionmentioning

confidence: 54%

The Dynamic SUMOylation Changes and Their Potential Role in the Senescence of APOE4 Mice

Xu,

Cai,

Sang

et al. 2023

Biomedicines

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“…As a main sirtuin located in mitochondria, SIRT3 involves in mitochondrial fatty acid oxidation, mitochondrial biogenesis, and oxidative phosphorylation in skeletal muscle. 40,41 Previous study indicated that the activation of SIRT3 could ameliorate muscle injury via promoting mitochondrial biogenesis. 42 In addition, overexpression of SIRT3 showed higher energy expenditure and lower incidence of muscle atrophy, which was achieved by activating the downstream PPARδ and AMPK.…”

Section: Discussionmentioning

confidence: 65%

5-Heptadecylresorcinol Ameliorates Obesity-Associated Skeletal Muscle Mitochondrial Dysfunction through SIRT3-Mediated Mitophagy

Wang,

Li,

Yang

et al. 2023

J. Agric. Food Chem.

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Skeletal muscle dysfunction caused by obesity is characterized by the decline in mitochondrial content and function. 5-Heptadecylresorcinol (AR-C17) is a specific bioactive component derived from whole wheat and rye, which has been evidenced to improve obesity-associated skeletal muscle dysregulation. However, the mechanism underlying its protective activity requires further exploration. Herein, we found that AR-C17 (5, 10, and 20 μM) intervention reversed PA-induced (0.5 mM) reduction in mitochondrial content, mitochondrial membrane potential, and mitochondrial energy metabolism in C2C12 cells. Meanwhile, AR-C17 evidently alleviated PA-mediated myotube mitochondrial dysfunction via elevating mitochondria autophagy flux and upregulating the expression level of autophagy-related protein, while this effect was abolished by an autophagy inhibitor (3-MA). Further analysis showed that SIRT3-FOXO3A-PINK-Parkin-mediated mitophagy was involved in the modulation of myocyte mitochondrial dysfunction by AR-C17. In addition, AR-C17 administration (30 and 150 mg/kg/day) significantly improved high-fat-diet-induced mitochondrial dysregulation in mice skeletal muscle tissue via SIRT3-dependent mitophagy. Our findings indicate that skeletal muscle cells are responsive to AR-C17, which improves myogenesis and mitophagy in vitro and in vivo.

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“…SIRT3, a nicotinamide adenine dinucleotide (NAD + )-dependent enzyme, was reported to play a key role in the modulation of mitochondrial function and is considered a therapeutic target of neurodegeneration diseases [47]. It has been illustrated that SIRT3 activation presented the neuroprotective effect, reducing the beta-amyloid (Aβ) and Tau accumulation which contributed to oxidative neurotoxicity in the brain tissues of AD animals [48].…”

Section: Discussionmentioning

confidence: 99%

Piceatannol Protects PC-12 Cells against Oxidative Damage and Mitochondrial Dysfunction by Inhibiting Autophagy via SIRT3 Pathway

Liu,

Mai,

Yang

et al. 2023

Nutrients

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Oxidative stress has been identified as a major cause of cellular injury in a variety of neurodegenerative disorders. This study aimed to investigate the cytoprotective effects of piceatannol on hydrogen peroxide (H2O2)-induced pheochromocytoma-12 (PC-12) cell damage and explore the underlying mechanisms. Our findings indicated that piceatannol pre-treatment significantly attenuated H2O2-induced PC-12 cell death. Furthermore, piceatannol effectively improved mitochondrial content and mitochondrial function, including enhancing mitochondrial reactive oxygen species (ROS) elimination capacity and increasing mitochondrial transcription factor (TFAM), peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α) and mitochondria Complex IV expression. Meanwhile, piceatannol treatment inhibited mitochondria-mediated autophagy as demonstrated by restoring mitochondrial membrane potential, reducing autophagosome formation and light chain 3B II/I (LC3B II/I) and autophagy-related protein 5 (ATG5) expression level. The protein expression level of SIRT3 was significantly increased by piceatannol in a concentration-dependent manner. However, the cytoprotective effect of piceatannol was dramatically abolished by sirtuin 3 (SIRT3) inhibitor, 3-(1H-1,2,3-Triazol-4-yl) pyridine (3-TYP), which led to an exacerbated mitochondrial dysfunction and autophagy in PC-12 cells under oxidative stress. In addition, the autophagy activator (rapamycin) abrogated the protective effects of piceatannol on PC-12 cell death. These findings demonstrated that piceatannol could alleviate PC-12 cell oxidative damage and mitochondrial dysfunction by inhibiting autophagy via the SIRT3 pathway.

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Internship: A time to prioritise

Cited by 6 publications

References 0 publications

The Dynamic SUMOylation Changes and Their Potential Role in the Senescence of APOE4 Mice

The Dynamic SUMOylation Changes and Their Potential Role in the Senescence of APOE4 Mice

5-Heptadecylresorcinol Ameliorates Obesity-Associated Skeletal Muscle Mitochondrial Dysfunction through SIRT3-Mediated Mitophagy

Piceatannol Protects PC-12 Cells against Oxidative Damage and Mitochondrial Dysfunction by Inhibiting Autophagy via SIRT3 Pathway

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