Comparative proteomic analysis identifies biomarkers for renal aging

Yi, Meiqi; Ma, Yingying; Zhu, Songbiao; Luo, Chengting; Chen, Yuling; Wang, Qingtao; Deng, Haiteng

doi:10.18632/aging.104007

Cited by 12 publications

(14 citation statements)

References 44 publications

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“…In other studies, researchers combined a variety of technologies, such as optogenetics, synthetic biology ( Padmanabhan et al, 2019 ; Hemmati et al, 2020 ; Yi et al, 2020 ; Zhang et al, 2020 ), for the first time to achieve far red light to control the expression of genomic genes. The far-red light-regulated CRISPR-dCas9 endogenous gene transcription activation device was developed for the first time ( Gjaltema and Schulz, 2018 ), which successfully induced the pluripotent stem cells into functional neural cells ( Shao et al, 2018 ).…”

Section: Optogenetic Research Methodsmentioning

confidence: 99%

The Roles of Optogenetics and Technology in Neurobiology: A Review

Chen

Liang

et al. 2022

Front. Aging Neurosci.

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Optogenetic is a technique that combines optics and genetics to control specific neurons. This technique usually uses adenoviruses that encode photosensitive protein. The adenovirus may concentrate in a specific neural region. By shining light on the target nerve region, the photosensitive protein encoded by the adenovirus is controlled. Photosensitive proteins controlled by light can selectively allow ions inside and outside the cell membrane to pass through, resulting in inhibition or activation effects. Due to the high precision and minimally invasive, optogenetics has achieved good results in many fields, especially in the field of neuron functions and neural circuits. Significant advances have also been made in the study of many clinical diseases. This review focuses on the research of optogenetics in the field of neurobiology. These include how to use optogenetics to control nerve cells, study neural circuits, and treat diseases by changing the state of neurons. We hoped that this review will give a comprehensive understanding of the progress of optogenetics in the field of neurobiology.

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Section: Optogenetic Research Methodsmentioning

confidence: 99%

The Roles of Optogenetics and Technology in Neurobiology: A Review

Chen

Liang

et al. 2022

Front. Aging Neurosci.

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“…Protein SSG has been reported to cause a decrease (in most cases) or increase in the activity of proteins that are involved in energy metabolism and glycolysis, gene expression, signaling, calcium-dependent channels, apoptosis and autophagy, cell structure and dynamics, and protein folding [ 48 , 99 , 100 ]. Dynamic changes of protein SSGs were also shown to be prevalent in oxidative stress-associated disease progression, thus providing insights in clinical applications, including discovery of biomarkers, molecular targets for drug development, or therapeutic interventions [ 48 , 77 , 101 , 102 , 103 , 104 ].…”

Section: Functional Roles Of S-glutathionylationmentioning

confidence: 99%

Defining the S-Glutathionylation Proteome by Biochemical and Mass Spectrometric Approaches

Zhang

Day

et al. 2022

Antioxidants

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Protein S-glutathionylation (SSG) is a reversible post-translational modification (PTM) featuring the conjugation of glutathione to a protein cysteine thiol. SSG can alter protein structure, activity, subcellular localization, and interaction with small molecules and other proteins. Thus, it plays a critical role in redox signaling and regulation in various physiological activities and pathological events. In this review, we summarize current biochemical and analytical approaches for characterizing SSG at both the proteome level and at individual protein levels. To illustrate the mechanism underlying SSG-mediated redox regulation, we highlight recent examples of functional and structural consequences of SSG modifications. Finally, we discuss the analytical challenges in characterizing SSG and the thiol PTM landscape, future directions for understanding of the role of SSG in redox signaling and regulation and its interplay with other PTMs, and the potential role of computational approaches to accelerate functional discovery.

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“…Nicotinamide adenine dinucleotide (NAD + ) is a necessary cofactor for many biological redox processes and a substrate for SIRTs. , NMN is directly transformed into NAD + after one-step adenyltransferation catalyzed by NMNAT, and NMN treatment reversed age-related protein hyperacetylation in aged mouse liver . Studies demonstrated that the long-term NMN supplementation ameliorated metabolic disorders, ,, and NMN administration attenuated brain injury in intracerebral hemorrhage mouse models, ameliorated CCL4-induced liver fibrosis, and improved kidney peroxisomal functions in aged mouse. − However, the functions and mechanisms of NMN supplementation on aged liver are unknown. Considering the antioxidant functions of NMN, we propose that NMN can be an efficient way to restore redox homeostasis in aged mouse liver.…”

Section: Introductionmentioning

confidence: 99%

Nicotinamide Mononucleotide Administration Restores Redox Homeostasis via the Sirt3–Nrf2 Axis and Protects Aged Mice from Oxidative Stress-Induced Liver Injury

et al. 2022

Self Cite

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Altered adaptive homeostasis contributes to aging and lifespan regulation. In the present study, to characterize the mechanism of aging in mouse liver, we performed quantitative proteomics and found that the most upregulated proteins were related to the oxidation–reduction process. Further analysis revealed that malondialdehyde (MDA) and protein carbonyl (PCO) levels were increased, while nuclear Nrf2 and downstream genes were significantly increased, indicating that oxidative stress induced Nrf2 activation in aged mouse liver. Importantly, nicotinamide mononucleotide (NMN) administration decreased the oxidative stress and the nuclear Nrf2 and Nrf2 downstream gene levels. Indeed, aged mice treated with NMN improved stress resistance against acetaminophen (APAP)-induced liver injury, indicating that NMN restored Nrf2-mediated adaptive homeostasis. Further studies found that NMN increased Sirt3 activities to deacetylate age-associated acetylation at K68 and K122 in Sod2, while its effects on nuclear Nrf2 levels were diminished in Sirt3-deficient mice, suggesting that NMN-enhanced adaptive homeostasis was Sirt3-dependent. Taken together, we demonstrated that Nrf2-regulated adaptive homeostasis was decreased in aged mouse liver and NMN supplementation restored liver redox homeostasis via the Sirt3–Nrf2 axis and protected aged liver from oxidative stress-induced injury.

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Comparative proteomic analysis identifies biomarkers for renal aging

Cited by 12 publications

References 44 publications

The Roles of Optogenetics and Technology in Neurobiology: A Review

The Roles of Optogenetics and Technology in Neurobiology: A Review

Defining the S-Glutathionylation Proteome by Biochemical and Mass Spectrometric Approaches

Nicotinamide Mononucleotide Administration Restores Redox Homeostasis via the Sirt3–Nrf2 Axis and Protects Aged Mice from Oxidative Stress-Induced Liver Injury

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