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      Anti-aging effect of β-carotene through regulating the KAT7-P15 signaling axis, inflammation and oxidative stress process


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          Research on aging is growing as the elderly make up a greater share of the population, focusing on reversing and inhibiting the aging process. The exhaustion and senescence of stem cells are the fundamental drivers behind aging. β-Carotene has been depicted to have many biological functions, and we speculate that it may have an anti-aging effect.


          Firstly, the anti-aging property of β-carotene was investigated in vitro using mesenchymal stem cells (MSCs) induced by H 2O 2. The anti-aging effect was characterized using Western-bloting, confocal laser scanning microscopy, indirect immunofluorescence, and immunohistochemistry. The anti-aging property was also tested in vivo using aged mice.


          The in vitro experiment revealed that β-carotene could relieve the aging of MSCs, as evidenced by a series of aging marker molecules such as p16 and p21. β-Carotene appeared to inhibit aging by regulating the KAT7-P15 signaling axis. The in vivo experiment revealed that β-carotene treatment has significantly down-regulated the aging level of tissues and organs.


          In this work, we explored the anti-aging effect of β-carotene in vivo and in vitro. The experimental results indicate that β-carotene may be an important potential anti-aging molecule, which can be used as a drug or in functional food to treat aging in the future.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s11658-022-00389-7.

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          Most cited references31

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          Aging of mesenchymal stem cell in vitro

          Background A hot new topic in medical treatment is the use of mesenchymal stem cells (MSC) in therapy. The low frequency of this subpopulation of stem cells in bone marrow (BM) necessitates their in vitro expansion prior to clinical use. We evaluated the effect of long term culture on the senescence of these cells. Results The mean long term culture was 118 days and the mean passage number was 9. The average number of PD decreased from 7.7 to 1.2 in the 10th passage. The mean telomere length decreased from 9.19 Kbp to 8.7 kbp in the 9th passage. Differentiation potential dropped from the 6th passage on. The culture's morphological abnormalities were typical of the Hayflick model of cellular aging. Conclusion We believe that MSC enter senescence almost undetectably from the moment of in vitro culturing. Simultaneously these cells are losing their stem cell characteristics. Therefore, it is much better to consider them for cell and gene therapy early on.
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            Molecular and physiological manifestations and measurement of aging in humans

            Summary Biological aging is associated with a reduction in the reparative and regenerative potential in tissues and organs. This reduction manifests as a decreased physiological reserve in response to stress (termed homeostenosis) and a time‐dependent failure of complex molecular mechanisms that cumulatively create disorder. Aging inevitably occurs with time in all organisms and emerges on a molecular, cellular, organ, and organismal level with genetic, epigenetic, and environmental modulators. Individuals with the same chronological age exhibit differential trajectories of age‐related decline, and it follows that we should assess biological age distinctly from chronological age. In this review, we outline mechanisms of aging with attention to well‐described molecular and cellular hallmarks and discuss physiological changes of aging at the organ‐system level. We suggest methods to measure aging with attention to both molecular biology (e.g., telomere length and epigenetic marks) and physiological function (e.g., lung function and echocardiographic measurements). Finally, we propose a framework to integrate these molecular and physiological data into a composite score that measures biological aging in humans. Understanding the molecular and physiological phenomena that drive the complex and multifactorial processes underlying the variable pace of biological aging in humans will inform how researchers assess and investigate health and disease over the life course. This composite biological age score could be of use to researchers seeking to characterize normal, accelerated, and exceptionally successful aging as well as to assess the effect of interventions aimed at modulating human aging.
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              IL1- and TGFβ-Nox4 signaling, oxidative stress and DNA damage response are shared features of replicative, oncogene-induced, and drug-induced paracrine ‘Bystander senescence’

              Many cancers arise at sites of infection and inflammation. Cellular senescence, a permanent state of cell cycle arrest that provides a barrier against tumorigenesis, is accompanied by elevated proinflammatory cytokines such as IL1, IL6, IL8 and TNFα. Here we demonstrate that media conditioned by cells undergoing any of the three main forms of senescence, i.e. replicative, oncogene- and drug-induced, contain high levels of IL1, IL6, and TGFb capable of inducing reactive oxygen species (ROS)-mediated DNA damage response (DDR). Persistent cytokine signaling and activated DDR evoke senescence in normal bystander cells, accompanied by activation of the JAK/STAT, TGFβ/SMAD and IL1/NFκB signaling pathways. Whereas inhibition of IL6/STAT signaling had no effect on DDR induction in bystander cells, inhibition of either TGFβ/SMAD or IL1/NFκB pathway resulted in decreased ROS production and reduced DDR in bystander cells. Simultaneous inhibition of both TGFβ/SMAD and IL1/NFκB pathways completely suppressed DDR indicating that IL1 and TGFβ cooperate to induce and/or maintain bystander senescence. Furthermore, the observed IL1- and TGFβ-induced expression of NAPDH oxidase Nox4 indicates a mechanistic link between the senescence-associated secretory phenotype (SASP) and DNA damage signaling as a feature shared by development of all major forms of paracrine bystander senescence.

                Author and article information

                Cell Mol Biol Lett
                Cell Mol Biol Lett
                Cellular & Molecular Biology Letters
                BioMed Central (London )
                8 October 2022
                8 October 2022
                : 27
                : 86
                [1 ]GRID grid.440601.7, ISNI 0000 0004 1798 0578, Intervention and Cell Therapy Center, , Peking University Shenzhen Hospital, ; Shenzhen, Guangdong 518036 People’s Republic of China
                [2 ]GRID grid.440601.7, ISNI 0000 0004 1798 0578, Department of Minimally Invasion Intervention, , Peking University Shenzhen Hospital, ; Shenzhen, Guangdong 518036 People’s Republic of China
                [3 ]GRID grid.440601.7, ISNI 0000 0004 1798 0578, Department of Infectious Disease, , Peking University Shenzhen Hospital, ; Shenzhen, Guangdong 518036 People’s Republic of China
                [4 ]GRID grid.144022.1, ISNI 0000 0004 1760 4150, College of Veterinary Medicine, , Northwest A&F University, ; Yangling, 712100 China
                [5 ]GRID grid.440601.7, ISNI 0000 0004 1798 0578, Scientific and Resaerch Dept., , Peking University Shenzhen Hospital, ; Shenzhen, Guangdong 518036 People’s Republic of China
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                : 19 May 2022
                : 19 September 2022
                Funded by: FundRef http://dx.doi.org/10.13039/501100012151, Sanming Project of Medicine in Shenzhen;
                Award ID: 201612071
                Award Recipient :
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                © The Author(s) 2022

                β-carotene,aging,stem cells,kat7-p15 signaling axis
                β-carotene, aging, stem cells, kat7-p15 signaling axis


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