The Role of SIRT3 in the Osteoporosis

Hu, Siwang; Wang, Shuangshuang

doi:10.3389/fendo.2022.893678

Cited by 12 publications

(8 citation statements)

References 121 publications

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“…Similarly, a previous study demonstrates that SIRT5 deletion promotes obesity-associated osteoarthritis development [ 24 ]. In addition, the role of other members of the SIRT family in bone-related diseases has also been described [ 26 , 27 ]. Interestingly, we found that low level of SIRT5 was also associated with tumors that are not primary chordoma (6 out of 13), suggesting that other primary tumors may have a low level of SIRT5 or that other primary tumors may have a high level of SIRT5 while the SIRT5 level was decreased when progressing and metastasizing.…”

Section: Discussionmentioning

confidence: 99%

SIRT5 promote malignant advancement of chordoma by regulating the desuccinylation of c-myc

Jiang,

Huang,

Chen

et al. 2024

BMC Cancer

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Chordoma is a relatively rare and locally aggressive malignant tumor. Sirtuin (SIRT)5 plays pivotal roles in various tumors, but the role of SIRT5 in chordoma has not been found. This study was performed to investigate the regulatory effects of SIRT5 on cell proliferation, migration, and invasion and the underlying mechanism in chordoma. A xenograft tumor mouse model was established to assess tumor growth. Reverse transcription-quantitative polymerase chain reaction was used to analyze the mRNA levels of SIRT5 and c-myc. The effects of SIRT5 and c-myc on cell proliferation, migration, and invasion of chordoma cells were detected by cell counting kit-8, colony formation, and Transwell assays. The interaction between SIRT5 and c-myc was evaluated by co-immunoprecipitation (IP) assay. The succinylation of c-myc was analyzed by IP and Western blot. The results showed that SIRT5 expression was upregulated in chordoma tissues and cells. SIRT5 interacted with c-myc to inhibit the succinylation of c-myc at K369 site in human embryonic kidney (HEK)-293T cells. Silencing of SIRT5 suppressed the cell proliferation, migration, and invasion of chordoma cells, while the results were reversed after c-myc overexpression. Moreover, silencing SIRT5 suppressed tumor growth in mice. These findings suggested that SIRT5 promoted the malignant advancement of chordoma by regulating the desuccinylation of c-myc.

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Section: Discussionmentioning

confidence: 99%

SIRT5 promote malignant advancement of chordoma by regulating the desuccinylation of c-myc

Jiang,

Huang,

Chen

et al. 2024

BMC Cancer

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“…Osteoporosis is a common aging-related disease characterized by decreased bone mass and fragility fractures, and places a huge burden on society ( Hu and Wang, 2022 ). The kl/kl mice exhibit a state of low turnover involving formation and resorption of bone, similar to humans ( Kuro-o et al, 1997 ).…”

Section: Discussionmentioning

confidence: 99%

Impact of Ninjin’yoeito on frailty and short life in klotho-hypomorphic (kl/kl) mice

Amitani

Chiba²,

Amitani³

et al. 2022

Front. Pharmacol.

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With the recent aging of society, the prevention of frailty has become an important issue because people desire both a long and healthy lifespan. Klotho-hypomorphic (kl/kl) mice are known to show phenotypes of premature aging. Ninjin’yoeito (NYT) is a traditional Japanese Kampo medicine used to treat patients with vulnerable constitution, fatigue or physical exhaustion caused by aging and illness. Recent studies have reported the potential efficacy of NYT against frailty. We therefore evaluated the effect of NYT on the gait function, activity, the histopathological status of organs and survival using kl/kl mice as a model of aging-related frailty. Two sets of 28-day-old male kl/kl mice were assigned to the vehicle (non-treated; NT), 3% or 5% NYT dietary groups. One set of groups (NT, n = 18; 3% NYT, n = 11; 5% NYT, n = 11) was subjected to the analysis of free walking, rotarod, and spontaneous activity tests at approximately 58 days old. Thereafter, we measured triceps surae muscles weight and myofiber cross-sectional area (CSA), and quantified its telomere content. In addition, we evaluated bone strength and performed histopathological examinations of organs. Survival was measured in the second set of groups (NT, 3% NYT and 5% NYT group, n = 8 each). In the walking test, several indicators such as gait velocity were improved in the NYT 3% group. Similar results were obtained for the latency to fall in the rotarod test and spontaneous motor activity. Triceps muscle mass, CSA and its telomere content were significantly improved in the NYT 3% group. Bone density, pulmonary alveolus destruction and testicular atrophy were also significantly improved in the NYT 3% group. Survival rate and body weight were both significantly improved in the NYT3% group compared with those in the NT group. Continuous administration of NYT from the early stage of aging improved not only gait performance, but also the survival in the aging-related frailty model. This effect may be associated with the improvements in aging-related organ changes such as muscle atrophy. Intervention with NYT against the progression of frailty may contribute to a longer, healthier life span among the elderly individuals.

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“…Mice lacking SIRT3 have significantly shortened lifespans (Benigni et al, 2019 ) and spontaneously develop aging‐related diseases. Deletion of SIRT3 has a deleterious effect on mitochondrial biogenesis and function, which plays an important role in several age‐related diseases (Cao, Zhao, et al, 2022 ; Hu & Wang, 2022 ). Increased SIRT6 activity also correlates with increased lifespan among species, a phenotype attributed to its effect on protection from DNA damage (Korotkov et al, 2021 ; Taylor et al, 2022 ; Tian et al, 2019 ).…”

Section: Nad Metabolism In Agingmentioning

confidence: 99%

NAD metabolism: Role in senescence regulation and aging

Chini,

Cordeiro,

Tran

et al. 2023

Aging Cell

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The geroscience hypothesis proposes that addressing the biology of aging could directly prevent the onset or mitigate the severity of multiple chronic diseases. Understanding the interplay between key aspects of the biological hallmarks of aging is essential in delivering the promises of the geroscience hypothesis. Notably, the nucleotide nicotinamide adenine dinucleotide (NAD) interfaces with several biological hallmarks of aging, including cellular senescence, and changes in NAD metabolism have been shown to be involved in the aging process. The relationship between NAD metabolism and cellular senescence appears to be complex. On the one hand, the accumulation of DNA damage and mitochondrial dysfunction induced by low NAD+ can promote the development of senescence. On the other hand, the low NAD+ state that occurs during aging may inhibit SASP development as this secretory phenotype and the development of cellular senescence are both highly metabolically demanding. However, to date, the impact of NAD+ metabolism on the progression of the cellular senescence phenotype has not been fully characterized. Therefore, to explore the implications of NAD metabolism and NAD replacement therapies, it is essential to consider their interactions with other hallmarks of aging, including cellular senescence. We propose that a comprehensive understanding of the interplay between NAD boosting strategies and senolytic agents is necessary to advance the field.

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The Role of SIRT3 in the Osteoporosis

Cited by 12 publications

References 121 publications

SIRT5 promote malignant advancement of chordoma by regulating the desuccinylation of c-myc

SIRT5 promote malignant advancement of chordoma by regulating the desuccinylation of c-myc

Impact of Ninjin’yoeito on frailty and short life in klotho-hypomorphic (kl/kl) mice

NAD metabolism: Role in senescence regulation and aging

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