Mitochondrial sirtuins, metabolism, and aging

Ji, Zhejun; Liu, Guanghui; Qu, Jing

doi:10.1016/j.jgg.2021.11.005

Cited by 89 publications

(43 citation statements)

References 157 publications

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“…SIRT3 encodes the proteins involved in longevity by promoting organelle renewal and senescence delaying 18,19 . SIRT3 is an important factor participating in mitochondrial synthesis 20 . Mitochondria is the metabolic factories in cells, and SIRT3 promotes cellular metastasis by enhancing mitochondrial function.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

et al. 2022

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Accumulation of lipid substances decreased the activity of osteoblasts. Trehalose is a typical stress metabolite to form a protective membrane on cell surface which has been demonstrated to regulate lipid metabolism. This activity of Trehalose indicates the potential effect of osteoporosis treatment. Our study aimed to determine the therapeutic effect of Trehalose in high fat-induced osteoporosis. We used palmitic acid (PA) to mimic the state of high fat and observed the apoptosis ratio of osteoblasts increased. After adding Trehalose, the apoptosis ratio decreased obviously. Autophagy is a regulatory means involved in the process of apoptosis.We detected the autophagy protein and found that the expression of Beclin-1, Atg5, and LC3 II increased, and p62 decreased after Trehalose treatment. When adding an autophagy inhibitor (3-MA), the expression of Beclin-1, Atg5, and LC3 II decreased, and p62 increased. These results indicated autophagy was an important factor involved in the preventive effect of Trehalose in PA-induced apoptosis. SIRT3 is a mitochondrial gene that can inhibit apoptosis, which has been reported to promote autophagy. We used SIRT3-siRNA to silence the expression of SIRT3 and found the effect of Trehalose was counteracted. The apoptosis ratio increased and the expression of Beclin-1, Atg5, and LC3 II decreased, p62 increased. Additionally, we also fed the mice with a high-fat diet (HFD) and intragastrical Trehalose. The results showed that Trehalose could inhibit the bone mass loss with HFD. Our study revealed the effect and mechanism of Trehalose in the treatment of osteoporosis.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

et al. 2022

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“… 57 However, SIRT5 loss in HEK293 cells is associated with a reduced pyruvate-dependent cellular respiration, 89 thus suggesting that the role of SIRT5 in glucose metabolism is context-dependent. 90 …”

Section: Biological Activities and Disease Relevance Of Sirt5mentioning

confidence: 99%

Therapeutic Potential and Activity Modulation of the Protein Lysine Deacylase Sirtuin 5

et al. 2022

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Sirtiun 5 (SIRT5) is a NAD + -dependent protein lysine deacylase primarily located in mitochondria. SIRT5 displays an affinity for negatively charged acyl groups and mainly catalyzes lysine deglutarylation, desuccinylation, and demalonylation while possessing weak deacetylase activity. SIRT5 substrates play crucial roles in metabolism and reactive oxygen species (ROS) detoxification, and SIRT5 activity is protective in neuronal and cardiac physiology. Moreover, SIRT5 exhibits a dichotomous role in cancer, acting as context-dependent tumor promoter or suppressor. Given its multifaceted activity, SIRT5 is a promising target in the design of activators or inhibitors that might act as therapeutics in many pathologies, including cancer, cardiovascular disorders, and neurodegeneration. To date, few cellular-active peptide-based SIRT5 inhibitors (SIRT5i) have been described, and potent and selective small-molecule SIRT5i have yet to be discovered. In this perspective, we provide an outline of SIRT5’s roles in different biological settings and describe SIRT5 modulators in terms of their mode of action, pharmacological activity, and structure–activity relationships.

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“…Due to the widespread interest in understanding the biology of aging, numerous signaling pathways sensitive to NAD+(H) perturbations have received increased scientific interest. Much of the renewed interest in NAD over the last decade can be attributed to the Sirtuins (SIRTs), a family of NAD+-dependent protein deacetylases with remarkable abilities in promoting longevity and alleviating aging-associated diseases [ 13 ]. Meanwhile, similar to the exercise-sensing effect of NAD, SIRTs are also closely related to exercise [ 14 ].…”

Section: Sirt3: Big Picture Overviewmentioning

confidence: 99%

“…Again, SIRT3 is the only SIRT that positively impacts human aging, as numerous studies have linked SIRT3 to longevity in humans and rodents [ 13 , 21 ]. Over the past decade, there has been an expansion of research exploring the therapeutic potential of SIRT3 [ 1 ].…”

Section: Sirt3: Big Picture Overviewmentioning

confidence: 99%

The Role of SIRT3 in Exercise and Aging

Zhou

Pinho

et al. 2022

Cells

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The health benefits of regular exercise are well established. Nonetheless, the molecular mechanism(s) responsible for exercise-induced health benefits remain a topic of debate. One of the key cell-signaling candidates proposed to provide exercise-induced benefits is sirtuin 3 (SIRT3). SIRT3, an NAD+ dependent mitochondrial deacetylase, positively modulates many cellular processes, including energy metabolism, mitochondrial biogenesis, and protection against oxidative stress. Although the exercise-induced change in SIRT3 signaling is a potential mechanism contributing to the health advantages of exercise on aging, studies investigating the impact of exercise on SIRT3 abundance in cells provide conflicting results. To resolve this conundrum, this narrative review provides a detailed analysis of the role that exercise-induced changes in SIRT3 play in providing the health and aging benefits associated with regular physical activity. We begin with an overview of SIRT3 function in cells followed by a comprehensive review of the impact of exercise on SIRT3 expression in humans and other mammalians. We then discuss the impact of SIRT3 on aging, followed by a thorough analysis of the cell-signaling links between SIRT3 and exercise-induced adaptation. Notably, to stimulate future research, we conclude with a discussion of key unanswered questions related to exercise, aging, and SIRT3 expression.

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Mitochondrial sirtuins, metabolism, and aging

Cited by 89 publications

References 157 publications

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

Therapeutic Potential and Activity Modulation of the Protein Lysine Deacylase Sirtuin 5

The Role of SIRT3 in Exercise and Aging

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