The Regulatory Effect of SIRT1 on Extracellular Microenvironment Remodeling

Wang, Zhuo; Guo, Wendong; Yi, Fei; Zhou, Tingting; Li, Xiaoman; Feng, Yanling; Guo, Qiqiang; Xu, Hongde; Song, Xiaoyu; Cao, Liu

doi:10.7150/ijbs.52619

Cited by 9 publications

(4 citation statements)

References 118 publications

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“…The expression of SIRT1 in oocytes increased in response to mitochondrial dysfunction in pigs and cows [11,12]; however, the level of responsive SIRT1 upregulation was low in oocytes derived from aged cows [12]. These results are consistent with the fact that AGEs inactivate SIRT1/NRF2 pathways [35]. Notably, we found that embryos derived from both aged and MGO-mice had increased SIRT1 expression levels.…”

Section: Discussionsupporting

confidence: 87%

Age-related advanced glycation end-product accumulation impairs mitochondrial regulation after vitrification

Ito

Iwata

2023

Biology of Reproduction

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Vitrification is an important assisted reproductive technology, although it induces mitochondrial dysfunction in embryos. Herein, we aimed to investigate whether age-associated accumulation of advanced glycation end-products (AGEs) in oocytes impairs the recovery of embryos from cryopreservation-induced mitochondrial dysfunction/damage. Mouse 8-cell stage embryos developed in vitro were vitrified and warmed and incubated up to the blastocyst stage. AGE levels in oocytes were higher in both aged mice and AGE accumulation mouse models (MGO-mice) than those in young and control mice. Additionally, the level of SIRT1 upregulation was lower for embryos of aged and MGO-mice than that for embryos of young and control mice. The highest mtDNA content was detected in blastocysts derived from vitrified embryos of aged and MGO-mice. The spent culture medium of blastocysts derived from both aged and MGO-mice contained higher mtDNA content than that of the blastocysts derived from young and control mice. EX527 increased mtDNA content in the spent culture medium of vitrified embryos derived from young mice. In addition, p62 aggregate levels were higher in vitrified embryos of control mice than those in vitrified embryos of MGO-mice. The SIRT1 activator, resveratrol, increased p62 aggregation levels in vitrified embryos derived from young and aged mice, whereas vitrification did not affect p62 aggregation levels in embryos from aged mice. Therefore, age-associated AGE accumulation induces decreased responsive SIRT1 upregulation following vitrified–warmed treatment and impairs mitochondrial quality control activity in vitrified embryos.

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Section: Discussionsupporting

confidence: 87%

Age-related advanced glycation end-product accumulation impairs mitochondrial regulation after vitrification

Ito

Iwata

2023

Biology of Reproduction

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“…However, SIRT1 not only affects intracellular homeostasis, but also participates in the remodeling of the extracellular microenvironment ( 101 ). SIRT1 and HIF-1α, as metabolic sensors of redox and oxygen, can modulate both innate and adaptive immune responses through metabolism-dependent and -independent ways ( 102 ).…”

Section: The Association Of Sirt1 With Hypoxia-induced Chemoresistance In Nsclcmentioning

confidence: 99%

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

Luo

et al. 2021

Front. Oncol.

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Resistance is the major cause of treatment failure and disease progression in non-small cell lung cancer (NSCLC). There is evidence that hypoxia is a key microenvironmental stress associated with resistance to cisplatin, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), and immunotherapy in solid NSCLCs. Numerous studies have contributed to delineating the mechanisms underlying drug resistance in NSCLC; nevertheless, the mechanisms involved in the resistance associated with hypoxia-induced molecular metabolic adaptations in the microenvironment of NSCLC remain unclear. Studies have highlighted the importance of posttranslational regulation of molecular mediators in the control of mitochondrial function in response to hypoxia-induced metabolic adaptations. Hypoxia can upregulate the expression of sirtuin 1 (SIRT1) in a hypoxia-inducible factor (HIF)-dependent manner. SIRT1 is a stress-dependent metabolic sensor that can deacetylate some key transcriptional factors in both metabolism dependent and independent metabolic pathways such as HIF-1α, peroxisome proliferator-activated receptor gamma (PPAR-γ), and PPAR-gamma coactivator 1-alpha (PGC-1α) to affect mitochondrial function and biogenesis, which has a role in hypoxia-induced chemoresistance in NSCLC. Moreover, SIRT1 and HIF-1α can regulate both innate and adaptive immune responses through metabolism-dependent and -independent ways. The objective of this review is to delineate a possible SIRT1/PGC-1α/PPAR-γ signaling-related molecular metabolic mechanism underlying hypoxia-induced chemotherapy resistance in the NSCLC microenvironment. Targeting hypoxia-related metabolic adaptation may be an attractive therapeutic strategy for overcoming chemoresistance in NSCLC.

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“…Some SIRTs can delocalize depending on the cell or tissue type, the developmental stage, metabolic status, and certain stress conditions [ 1 , 3 , 7 , 41 ]. The distribution of SIRTs in different subcellular compartments allows them to interact with a wide variety of transcription factors and to participate in the regulation of different metabolic processes, such as apoptosis, glucose homeostasis, insulin resistance, stress resistance, circadian rhythm, mitochondrial biogenesis, and DNA repair [ 1 , 2 , 3 , 4 , 43 ]. In addition, they play a key role in the development of inflammation and autophagy [ 56 ].…”

Section: The Function Structure and Regulation Of Sirtsmentioning

confidence: 99%

“…Human SIRTs form an evolutionarily conserved family of proteins that are ubiquitously expressed in all taxa. SIRTs are classified as NAD + dependent deacylases/mono-ADP ribosyltransferases that regulate numerous cellular functions, including metabolism, cell cycle, stress and longevity [ 1 , 2 , 3 , 4 ]. Their name comes from the first member of the family that was studied in Saccharomyces cerevisiae, which was characterized as “silent information regulator 2” (Sir2), because it appeared to be involved in gene transcription silencing [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

The Pleiotropic Function of Human Sirtuins as Modulators of Metabolic Pathways and Viral Infections

Alqarni

Foudah

Muharram

et al. 2021

Cells

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Sirtuins (SIRTs) are nicotinamide adenine dinucleotide-dependent histone deacetylases that incorporate complex functions in the mechanisms of cell physiology. Mammals have seven distinct members of the SIRT family (SIRT1-7), which play an important role in a well-maintained network of metabolic pathways that control and adapt the cell to the environment, energy availability and cellular stress. Until recently, very few studies investigated the role of SIRTs in modulating viral infection and progeny. Recent studies have demonstrated that SIRT1 and SIRT2 are promising antiviral targets because of their specific connection to numerous metabolic and regulatory processes affected during infection. In the present review, we summarize some of the recent progress in SIRTs biochemistry and their emerging function as antiviral targets. We also discuss the potential of natural polyphenol-based SIRT modulators to control their functional roles in several diseases including viral infections.

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The Regulatory Effect of SIRT1 on Extracellular Microenvironment Remodeling

Cited by 9 publications

References 118 publications

Age-related advanced glycation end-product accumulation impairs mitochondrial regulation after vitrification

Age-related advanced glycation end-product accumulation impairs mitochondrial regulation after vitrification

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

The Pleiotropic Function of Human Sirtuins as Modulators of Metabolic Pathways and Viral Infections

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