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  1. Article ; Online: Targeting aging cells improves survival.

    Cox, Lynne S / Lord, Janet M

    Science (New York, N.Y.)

    2021  Volume 373, Issue 6552, Page(s) 281–282

    MeSH term(s) Cellular Senescence
    Language English
    Publishing date 2021-08-27
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abi4474
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  2. Article ; Online: Linking interdisciplinary and multiscale approaches to improve healthspan-a new UK model for collaborative research networks in ageing biology and clinical translation.

    Cox, Lynne S / Faragher, Richard G A

    The lancet. Healthy longevity

    2022  Volume 3, Issue 5, Page(s) e318–e320

    MeSH term(s) Biology ; Interdisciplinary Studies ; Translations ; United Kingdom
    Language English
    Publishing date 2022-05-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2666-7568
    ISSN (online) 2666-7568
    DOI 10.1016/S2666-7568(22)00095-2
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  3. Article ; Online: The central role of DNA damage in immunosenescence.

    Kell, Loren / Simon, Anna Katharina / Alsaleh, Ghada / Cox, Lynne S

    Frontiers in aging

    2023  Volume 4, Page(s) 1202152

    Abstract: Ageing is the biggest risk factor for the development of multiple chronic diseases as well as increased infection susceptibility and severity of diseases such as influenza and COVID-19. This increased disease risk is linked to changes in immune function ... ...

    Abstract Ageing is the biggest risk factor for the development of multiple chronic diseases as well as increased infection susceptibility and severity of diseases such as influenza and COVID-19. This increased disease risk is linked to changes in immune function during ageing termed immunosenescence. Age-related loss of immune function, particularly in adaptive responses against pathogens and immunosurveillance against cancer, is accompanied by a paradoxical gain of function of some aspects of immunity such as elevated inflammation and increased incidence of autoimmunity. Of the many factors that contribute to immunosenescence, DNA damage is emerging as a key candidate. In this review, we discuss the evidence supporting the hypothesis that DNA damage may be a central driver of immunosenescence through senescence of both immune cells and cells of non-haematopoietic lineages. We explore why DNA damage accumulates during ageing in a major cell type, T cells, and how this may drive age-related immune dysfunction. We further propose that existing immunosenescence interventions may act, at least in part, by mitigating DNA damage and restoring DNA repair processes (which we term "genoprotection"). As such, we propose additional treatments on the basis of their evidence for genoprotection, and further suggest that this approach may provide a viable therapeutic strategy for improving immunity in older people.
    Language English
    Publishing date 2023-07-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 3076785-4
    ISSN 2673-6217 ; 2673-6217
    ISSN (online) 2673-6217
    ISSN 2673-6217
    DOI 10.3389/fragi.2023.1202152
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  4. Article ; Online: Intercellular Transfer of Mitochondria between Senescent Cells through Cytoskeleton-Supported Intercellular Bridges Requires mTOR and CDC42 Signalling.

    Walters, Hannah E / Cox, Lynne S

    Oxidative medicine and cellular longevity

    2021  Volume 2021, Page(s) 6697861

    Abstract: Cellular senescence is a state of irreversible cell proliferation arrest induced by various stressors including telomere attrition, DNA damage, and oncogene induction. While beneficial as an acute response to stress, the accumulation of senescent cells ... ...

    Abstract Cellular senescence is a state of irreversible cell proliferation arrest induced by various stressors including telomere attrition, DNA damage, and oncogene induction. While beneficial as an acute response to stress, the accumulation of senescent cells with increasing age is thought to contribute adversely to the development of cancer and a number of other age-related diseases, including neurodegenerative diseases for which there are currently no effective disease-modifying therapies. Non-cell-autonomous effects of senescent cells have been suggested to arise through the SASP, a wide variety of proinflammatory cytokines, chemokines, and exosomes secreted by senescent cells. Here, we report an additional means of cell communication utilised by senescent cells via large numbers of membrane-bound intercellular bridges-or tunnelling nanotubes (TNTs)-containing the cytoskeletal components actin and tubulin, which form direct physical connections between cells. We observe the presence of mitochondria in these TNTs and show organelle transfer through the TNTs to adjacent cells. While transport of individual mitochondria along single TNTs appears by time-lapse studies to be unidirectional, we show by differentially labelled co-culture experiments that organelle transfer through TNTs can occur between different cells of equivalent cell age, but that senescent cells, rather than proliferating cells, appear to be predominant mitochondrial donors. Using small molecule inhibitors, we demonstrate that senescent cell TNTs are dependent on signalling through the mTOR pathway, which we further show is mediated at least in part through the downstream actin-cytoskeleton regulatory factor CDC42. These findings have significant implications for the development of senomodifying therapies, as they highlight the need to account for local direct cell-cell contacts as well as the SASP in order to treat cancer and diseases of ageing in which senescence is a key factor.
    MeSH term(s) Cell Membrane Structures/metabolism ; Cells, Cultured ; Cellular Senescence ; Cytoskeleton/metabolism ; Fibroblasts/metabolism ; Fibroblasts/physiology ; Humans ; Mitochondria/metabolism ; Nanotubes ; TOR Serine-Threonine Kinases/metabolism ; cdc42 GTP-Binding Protein/metabolism
    Chemical Substances Tunneling Nanotubes ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; CDC42 protein, human (EC 3.6.5.2) ; cdc42 GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2021-07-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2021/6697861
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  5. Article ; Online: Interconnections between Inflammageing and Immunosenescence during Ageing.

    Teissier, Thibault / Boulanger, Eric / Cox, Lynne S

    Cells

    2022  Volume 11, Issue 3

    Abstract: Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately lead to the recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from the continued ... ...

    Abstract Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately lead to the recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from the continued presence of the initial trigger, or the dysfunction of signalling and/or effector pathways, is harmful to health. While successful ageing in older adults, including centenarians, is associated with low levels of inflammation, elevated inflammation increases the risk of poor health and death. Hence inflammation has been described as one of seven pillars of ageing. Age-associated sterile, chronic, and low-grade inflammation is commonly termed inflammageing-it is not simply a consequence of increasing chronological age, but is also a marker of biological ageing, multimorbidity, and mortality risk. While inflammageing was initially thought to be caused by "continuous antigenic load and stress", reports from the last two decades describe a much more complex phenomenon also involving cellular senescence and the ageing of the immune system. In this review, we explore some of the main sources and consequences of inflammageing in the context of immunosenescence and highlight potential interventions. In particular, we assess the contribution of cellular senescence to age-associated inflammation, identify patterns of pro- and anti-inflammatory markers characteristic of inflammageing, describe alterations in the ageing immune system that lead to elevated inflammation, and finally assess the ways that diet, exercise, and pharmacological interventions can reduce inflammageing and thus, improve later life health.
    MeSH term(s) Aged ; Aged, 80 and over ; Aging/physiology ; Biomarkers/metabolism ; Cellular Senescence/physiology ; Humans ; Immunosenescence ; Inflammation/metabolism
    Chemical Substances Biomarkers
    Language English
    Publishing date 2022-01-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11030359
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  6. Article ; Online: Interconnections between Inflammageing and Immunosenescence during Ageing

    Thibault Teissier / Eric Boulanger / Lynne S. Cox

    Cells, Vol 11, Iss 359, p

    2022  Volume 359

    Abstract: Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately lead to the recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from the continued ... ...

    Abstract Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately lead to the recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from the continued presence of the initial trigger, or the dysfunction of signalling and/or effector pathways, is harmful to health. While successful ageing in older adults, including centenarians, is associated with low levels of inflammation, elevated inflammation increases the risk of poor health and death. Hence inflammation has been described as one of seven pillars of ageing. Age-associated sterile, chronic, and low-grade inflammation is commonly termed inflammageing—it is not simply a consequence of increasing chronological age, but is also a marker of biological ageing, multimorbidity, and mortality risk. While inflammageing was initially thought to be caused by “continuous antigenic load and stress”, reports from the last two decades describe a much more complex phenomenon also involving cellular senescence and the ageing of the immune system. In this review, we explore some of the main sources and consequences of inflammageing in the context of immunosenescence and highlight potential interventions. In particular, we assess the contribution of cellular senescence to age-associated inflammation, identify patterns of pro- and anti-inflammatory markers characteristic of inflammageing, describe alterations in the ageing immune system that lead to elevated inflammation, and finally assess the ways that diet, exercise, and pharmacological interventions can reduce inflammageing and thus, improve later life health.
    Keywords ageing ; inflammation ; cytokines ; inflammageing ; immunosenescence ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Structural basis of the anti-ageing effects of polyphenolics: mitigation of oxidative stress.

    Rolt, Adam / Cox, Lynne S

    BMC chemistry

    2020  Volume 14, Issue 1, Page(s) 50

    Abstract: Ageing, and particularly the onset of age-related diseases, is associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Polyphenolic natural products such as stilbenoids, ... ...

    Abstract Ageing, and particularly the onset of age-related diseases, is associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Polyphenolic natural products such as stilbenoids, flavonoids and chalcones have been shown to be effective at ameliorating several age-related phenotypes, including oxidative stress, inflammation, impaired proteostasis and cellular senescence, both in vitro and in vivo. Here we aim to identify the structural basis underlying the pharmacology of polyphenols towards ROS and related biochemical pathways involved in age-related disease. We compile and describe SAR trends across different polyphenol chemotypes including stilbenoids, flavonoids and chalcones, review their different molecular targets and indications, and identify common structural ground between chemotypes and mechanisms of action. In particular, we focus on the structural requirements for the direct scavenging of reactive oxygen/nitrogen species such as radicals as well as coordination of a broader antioxidant response. We further suggest that it is important to consider multiple (rather than single) biological activities when identifying and developing new medicinal chemistry entities with utility in modulating complex biological properties such as cell ageing.
    Language English
    Publishing date 2020-08-10
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2661-801X
    ISSN (online) 2661-801X
    DOI 10.1186/s13065-020-00696-0
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  8. Article ; Online: Structural basis of the anti-ageing effects of polyphenolics

    Adam Rolt / Lynne S. Cox

    BMC Chemistry, Vol 14, Iss 1, Pp 1-

    mitigation of oxidative stress

    2020  Volume 13

    Abstract: Abstract Ageing, and particularly the onset of age-related diseases, is associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Polyphenolic natural products such as stilbenoids, ... ...

    Abstract Abstract Ageing, and particularly the onset of age-related diseases, is associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Polyphenolic natural products such as stilbenoids, flavonoids and chalcones have been shown to be effective at ameliorating several age-related phenotypes, including oxidative stress, inflammation, impaired proteostasis and cellular senescence, both in vitro and in vivo. Here we aim to identify the structural basis underlying the pharmacology of polyphenols towards ROS and related biochemical pathways involved in age-related disease. We compile and describe SAR trends across different polyphenol chemotypes including stilbenoids, flavonoids and chalcones, review their different molecular targets and indications, and identify common structural ground between chemotypes and mechanisms of action. In particular, we focus on the structural requirements for the direct scavenging of reactive oxygen/nitrogen species such as radicals as well as coordination of a broader antioxidant response. We further suggest that it is important to consider multiple (rather than single) biological activities when identifying and developing new medicinal chemistry entities with utility in modulating complex biological properties such as cell ageing.
    Keywords Ageing ; Aging ; Oxidative stress ; Inflammation ; Antioxidants ; Polyphenols ; Chemistry ; QD1-999
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: Crosstalk Between Senescent Bone Cells and the Bone Tissue Microenvironment Influences Bone Fragility During Chronological Age and in Diabetes.

    Teissier, Thibault / Temkin, Vladislav / Pollak, Rivka Dresner / Cox, Lynne S

    Frontiers in physiology

    2022  Volume 13, Page(s) 812157

    Abstract: Bone is a complex organ serving roles in skeletal support and movement, and is a source of blood cells including adaptive and innate immune cells. Structural and functional integrity is maintained through a balance between bone synthesis and bone ... ...

    Abstract Bone is a complex organ serving roles in skeletal support and movement, and is a source of blood cells including adaptive and innate immune cells. Structural and functional integrity is maintained through a balance between bone synthesis and bone degradation, dependent in part on mechanical loading but also on signaling and influences of the tissue microenvironment. Bone structure and the extracellular bone milieu change with age, predisposing to osteoporosis and increased fracture risk, and this is exacerbated in patients with diabetes. Such changes can include loss of bone mineral density, deterioration in micro-architecture, as well as decreased bone flexibility, through alteration of proteinaceous bone support structures, and accumulation of senescent cells. Senescence is a state of proliferation arrest accompanied by marked morphological and metabolic changes. It is driven by cellular stress and serves an important acute tumor suppressive mechanism when followed by immune-mediated senescent cell clearance. However, aging and pathological conditions including diabetes are associated with accumulation of senescent cells that generate a pro-inflammatory and tissue-destructive secretome (the SASP). The SASP impinges on the tissue microenvironment with detrimental local and systemic consequences; senescent cells are thought to contribute to the multimorbidity associated with advanced chronological age. Here, we assess factors that promote bone fragility, in the context both of chronological aging and accelerated aging in progeroid syndromes and in diabetes, including senescence-dependent alterations in the bone tissue microenvironment, and glycation changes to the tissue microenvironment that stimulate RAGE signaling, a process that is accelerated in diabetic patients. Finally, we discuss therapeutic interventions targeting RAGE signaling and cell senescence that show promise in improving bone health in older people and those living with diabetes.
    Language English
    Publishing date 2022-03-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.812157
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  10. Article ; Online: PCNA tightens its hold on the nucleus.

    Cox, Lynne S

    Cell cycle (Georgetown, Tex.)

    2015  Volume 14, Issue 17, Page(s) 2727–2728

    MeSH term(s) Histone-Lysine N-Methyltransferase/metabolism ; Humans ; Proliferating Cell Nuclear Antigen/metabolism ; Repressor Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Proliferating Cell Nuclear Antigen ; Repressor Proteins ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2015-07-15
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2015.1064699
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    In stock of ZB MED Cologne/Königswinter

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