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  1. Article ; Online: Slow and steady lives the longest.

    Morandini, Francesco / Seluanov, Andrei / Gorbunova, Vera

    Nature aging

    2024  Volume 4, Issue 1, Page(s) 7–9

    Language English
    Publishing date 2024-01-08
    Publishing country United States
    Document type Journal Article
    ISSN 2662-8465
    ISSN (online) 2662-8465
    DOI 10.1038/s43587-023-00554-3
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  2. Article: Introduction: Progression of the Science of Ageing.

    Gorbunova, Vera / Seluanov, Andrei

    Sub-cellular biochemistry

    2023  Volume 102, Page(s) 1–6

    Abstract: We outline the progression of ageing research from ancient history to present day geroscience. Calorie restriction, genetic mutations, and the involvement of the sirtuins are highlighted, along with pharmaceutical interventions, in particular rapamycin. ... ...

    Abstract We outline the progression of ageing research from ancient history to present day geroscience. Calorie restriction, genetic mutations, and the involvement of the sirtuins are highlighted, along with pharmaceutical interventions, in particular rapamycin. At the cellular level, replicative senescence and telomere shortening are presented in the history of ageing studies. We discuss the roles of macromolecular damage in ageing including damage to nuclear, and mitochondrial DNA, epigenetic and protein damage. The importance inflammation during ageing "inflammageing" is becoming increasingly recognized. Omics-based biomarkers are now proving to be a promising approach, along with comparative studies on long-lived animals. The science is getting closer to understanding the mechanisms of ageing and developing reliable interventions to improve human health.
    MeSH term(s) Humans ; Animals ; Cellular Senescence/genetics ; Aging/genetics ; DNA, Mitochondrial/genetics ; Mutation ; Mitochondria/genetics
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2023-01-04
    Publishing country United States
    Document type Journal Article
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-3-031-21410-3_1
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  3. Article ; Online: Editorial: DNA repair and interventions in aging.

    Brosh, Robert M / Moskalev, Alexey / Gorbunova, Vera

    Frontiers in aging

    2023  Volume 4, Page(s) 1306463

    Language English
    Publishing date 2023-12-05
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 3076785-4
    ISSN 2673-6217 ; 2673-6217
    ISSN (online) 2673-6217
    ISSN 2673-6217
    DOI 10.3389/fragi.2023.1306463
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  4. Article ; Online: Bat crazy iPSCs.

    Athar, Fathima / Seluanov, Andrei / Gorbunova, Vera

    Cell

    2023  Volume 186, Issue 5, Page(s) 901–903

    Abstract: Accelerating the development of tools for non-model animal research, Dejosez et al. report the generation of induced pluripotent stem cells (iPSCs) from bats using a modified Yamanaka protocol. Their study also reveals that bat genomes harbor diverse and ...

    Abstract Accelerating the development of tools for non-model animal research, Dejosez et al. report the generation of induced pluripotent stem cells (iPSCs) from bats using a modified Yamanaka protocol. Their study also reveals that bat genomes harbor diverse and unusually abundant endogenous retroviruses (ERVs) that are reactivated during iPSC reprogramming.
    MeSH term(s) Animals ; Chiroptera ; Induced Pluripotent Stem Cells ; Endogenous Retroviruses
    Language English
    Publishing date 2023-03-06
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.01.033
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  5. Article: Alpha-synuclein regulates the repair of genomic DNA double-strand breaks in a DNA-PK

    Rose, Elizabeth P / Osterberg, Valerie R / Banga, Jovin S / Gorbunova, Vera / Unni, Vivek K

    bioRxiv : the preprint server for biology

    2024  

    Abstract: α-synuclein (αSyn) is a presynaptic and nuclear protein that aggregates in important neurodegenerative diseases such as Parkinson's Disease (PD), Parkinson's Disease Dementia (PDD) and Lewy Body Dementia (LBD). Our past work suggests that nuclear αSyn ... ...

    Abstract α-synuclein (αSyn) is a presynaptic and nuclear protein that aggregates in important neurodegenerative diseases such as Parkinson's Disease (PD), Parkinson's Disease Dementia (PDD) and Lewy Body Dementia (LBD). Our past work suggests that nuclear αSyn may regulate forms of DNA double-strand break (DSB) repair in HAP1 cells after DNA damage induction with the chemotherapeutic agent bleomycin
    Language English
    Publishing date 2024-03-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.29.582819
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  6. Article ; Online: DNA damage and repair in age-related inflammation.

    Zhao, Yang / Simon, Matthew / Seluanov, Andrei / Gorbunova, Vera

    Nature reviews. Immunology

    2022  Volume 23, Issue 2, Page(s) 75–89

    Abstract: Genomic instability is an important driver of ageing. The accumulation of DNA damage is believed to contribute to ageing by inducing cell death, senescence and tissue dysfunction. However, emerging evidence shows that inflammation is another major ... ...

    Abstract Genomic instability is an important driver of ageing. The accumulation of DNA damage is believed to contribute to ageing by inducing cell death, senescence and tissue dysfunction. However, emerging evidence shows that inflammation is another major consequence of DNA damage. Inflammation is a hallmark of ageing and the driver of multiple age-related diseases. Here, we review the evidence linking DNA damage, inflammation and ageing, highlighting how premature ageing syndromes are associated with inflammation. We discuss the mechanisms by which DNA damage induces inflammation, such as through activation of the cGAS-STING axis and NF-κB activation by ATM. The triggers for activation of these signalling cascades are the age-related accumulation of DNA damage, activation of transposons, cellular senescence and the accumulation of persistent R-loops. We also discuss how epigenetic changes triggered by DNA damage can lead to inflammation and ageing via redistribution of heterochromatin factors. Finally, we discuss potential interventions against age-related inflammation.
    MeSH term(s) Humans ; DNA Damage ; Aging/genetics ; Cellular Senescence/genetics ; Inflammation/genetics ; Cell Death
    Language English
    Publishing date 2022-07-13
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-022-00751-y
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  7. Article ; Online: Long-lived fish in a big pond.

    Lu, J Yuyang / Seluanov, Andrei / Gorbunova, Vera

    Science (New York, N.Y.)

    2021  Volume 374, Issue 6569, Page(s) 824–825

    Abstract: The genetic drivers of extreme longevity in Pacific Ocean rockfish are identified. ...

    Abstract The genetic drivers of extreme longevity in Pacific Ocean rockfish are identified.
    MeSH term(s) Animals ; Fishes ; Ponds
    Language English
    Publishing date 2021-11-11
    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.abm3392
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  8. Article ; Online: 415 Line1 Derepression in Specific Retrotransposon Families in Aged Mice Leads to Cytosolic DNA and Increased Inflammation

    John Martinez / Matthew Simon / Andrei Seluanov / Vera Gorbunova

    Journal of Clinical and Translational Science, Vol 6, Pp 81-

    2022  Volume 81

    Abstract: OBJECTIVES/GOALS: The major objective of this project is two points. First, is to repeat and confirm previous observations that there is elevated cytosolic Line1 DNA in the cytoplasm of cells derived from old mice compared to young. Second is to identify ...

    Abstract OBJECTIVES/GOALS: The major objective of this project is two points. First, is to repeat and confirm previous observations that there is elevated cytosolic Line1 DNA in the cytoplasm of cells derived from old mice compared to young. Second is to identify which Line1s in the genome are contributing to this free DNA and test if targeting them rescues the age-related phenotype. METHODS/STUDY POPULATION: This project will focus on data collected from both tissues and primary cells derived from multiple tissues. Using cellular/tissue fractionation kits, we isolate specifically from the cytoplasm. This specificity is confirmed by western blotting. Measurement of the Line1 levels is measured by quantitative PCR. Subsequently, these cytoplasmic samples are sent off for sequencing in order to quantify the length of the free DNA in the cytoplasm and to identify which Line1 genomic families the cytosolic DNA originates. Additionally, FISH is utilized to visualize Line1 DNA in the cytoplasm of aged versus young cells RESULTS/ANTICIPATED RESULTS: We anticipate this research to confirm the hypothesis that extranuclear Line1 DNA accumulates with age in both tissues and primary fibroblasts. Additionally, we expect to be able to determine which specific families of genomic Line1 is driving this extranuclear DNA, which would suggest the active retrotransopable elements that are directly involved in this aging related phenotype. Assuming successful identification of such families, we can then target and silence these specific elements to determine not only if cytoplasmic Line1 in aged mice decreases, but additionally if the healthspan and/or lifespan of these mice improves DISCUSSION/SIGNIFICANCE: Dereoressed Line1s have been shown to be involved in detrimental phenotypes, including autoimmune disease, cancer, and inflammaging. Targeting retrotransposons, either directly through degradation of transcriptional product of LINE1s or indirectly by improving function of regulators, will be crucial in ablating aging phenotypes
    Keywords Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher Cambridge University Press
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Revelations About Aging and Disease from Unconventional Vertebrate Model Organisms.

    Zhao, Yang / Seluanov, Andrei / Gorbunova, Vera

    Annual review of genetics

    2021  Volume 55, Page(s) 135–159

    Abstract: Aging is a major risk factor for multiple diseases. Understanding the underlying mechanisms of aging would help to delay and prevent age-associated diseases. Short-lived model organisms have been extensively used to study the mechanisms of aging. However, ...

    Abstract Aging is a major risk factor for multiple diseases. Understanding the underlying mechanisms of aging would help to delay and prevent age-associated diseases. Short-lived model organisms have been extensively used to study the mechanisms of aging. However, these short-lived species may be missing the longevity mechanisms that are needed to extend the lifespan of an already long-lived species such as humans. Unconventional long-lived animal species are an excellent resource to uncover novel mechanisms of longevity and disease resistance. Here, we review mechanisms that evolved in nonmodel vertebrate species to counteract age-associated diseases. Some antiaging mechanisms are conserved across species; however, various nonmodel species also evolved unique mechanisms to delay aging and prevent disease. This variety of antiaging mechanisms has evolved due to the remarkably diverse habitats and behaviors of these species. We propose that exploring a wider range of unconventional vertebrates will provide important resources to study antiaging mechanisms that are potentially applicable to humans.
    MeSH term(s) Aging/genetics ; Animals ; Longevity/genetics ; Vertebrates/genetics
    Language English
    Publishing date 2021-08-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 207928-8
    ISSN 1545-2948 ; 0066-4170 ; 0066-4197
    ISSN (online) 1545-2948
    ISSN 0066-4170 ; 0066-4197
    DOI 10.1146/annurev-genet-071719-021009
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  10. Article ; Online: Sirtuin 6: linking longevity with genome and epigenome stability.

    Korotkov, Anatoly / Seluanov, Andrei / Gorbunova, Vera

    Trends in cell biology

    2021  Volume 31, Issue 12, Page(s) 994–1006

    Abstract: Sirtuin 6 (SIRT6) has been in the spotlight of aging research because progeroid phenotypes are associated with SIRT6 deficiency. SIRT6 has multiple molecular functions, including DNA repair and heterochromatin regulation, which position SIRT6 as a hub ... ...

    Abstract Sirtuin 6 (SIRT6) has been in the spotlight of aging research because progeroid phenotypes are associated with SIRT6 deficiency. SIRT6 has multiple molecular functions, including DNA repair and heterochromatin regulation, which position SIRT6 as a hub that regulates genome and epigenome stability. Genomic instability caused by persistent DNA damage and accumulating mutations, together with alterations in the epigenetic landscape and derepression of repetitive genetic elements, have emerged as mechanisms driving organismal aging. Enhanced levels of SIRT6 expression or activity provide avenues for rejuvenation strategies. This review focuses on the role of SIRT6 in the maintenance of genome and epigenome stability and its link to longevity. We propose a model where SIRT6 together with lamins control aging and rejuvenation by maintaining epigenetic silencing of repetitive elements.
    MeSH term(s) DNA Repair/genetics ; Epigenome ; Genome ; Humans ; Longevity/genetics ; Sirtuins/genetics ; Sirtuins/metabolism
    Chemical Substances SIRT6 protein, human (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2021-07-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2021.06.009
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