LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 7 of total 7

Search options

  1. Article ; Online: The Matrisome during Aging and Longevity: A Systems-Level Approach toward Defining Matreotypes Promoting Healthy Aging.

    Ewald, Collin Yvès

    Gerontology

    2019  Volume 66, Issue 3, Page(s) 266–274

    Abstract: Accumulation of damage is generally considered the cause of aging. Interventions that delay aging mobilize mechanisms that protect and repair cellular components. Consequently, research has been focused on studying the protective and homeostatic ... ...

    Abstract Accumulation of damage is generally considered the cause of aging. Interventions that delay aging mobilize mechanisms that protect and repair cellular components. Consequently, research has been focused on studying the protective and homeostatic mechanisms within cells. However, in humans and other multicellular organisms, cells are surrounded by extracellular matrices (ECMs), which are important for tissue structure, function, and intercellular communication. During aging, components of the ECM become damaged through fragmentation, glycation, crosslinking, and accumulation of protein aggregation, all of which contribute to age-related pathologies. Interestingly, placing senescent cells into a young ECM rejuvenates them. Furthermore, we found that many longevity-assurances pathways reactivate de novo synthesis of ECM proteins during aging. This raises the question of what constitutes a young ECM to reverse aging or maintain health? In order to make inroads to answering this question, I suggest a systems-level approach of quantifying the matrisome or ECM compositions reflecting health, pathology, or phenotype and propose a novel term, the "matreotype," to describe this. The matreotype is defined as the composition and modification of ECM or matrisome proteins associated with or caused by a phenotype, such as longevity, or a distinct and acute physiological state, as observed during aging or disease. Every cell type produces its unique ECM. Intriguingly, cancer-cell types can even be identified based on their unique ECM composition. Thus, the matreotype reflects cellular identity and physiological status. Defined matreotypes could be used as biomarkers or prognostic factors for disease or health status during aging with potential relevance for personalized medicine. Treatment with biologics that alter ECM-to-cell mechanotransduction might be a strategy to reverse age-associated pathologies. An understanding of how to reverse from an old to a young matreotype might point toward novel strategies to rejuvenate cells and help maintain tissue homeostasis to promote health during aging.
    MeSH term(s) Aging/physiology ; Extracellular Matrix/physiology ; Extracellular Matrix Proteins ; Healthy Aging/physiology ; Humans ; Longevity/physiology ; Mechanotransduction, Cellular ; Proteomics
    Chemical Substances Extracellular Matrix Proteins
    Language English
    Publishing date 2019-12-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000504295
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Removal of extracellular human amyloid beta aggregates by extracellular proteases in

    Jongsma, Elisabeth / Goyala, Anita / Mateos, José Maria / Ewald, Collin Yvès

    eLife

    2023  Volume 12

    Abstract: The amyloid beta (Aβ) plaques found in Alzheimer's disease (AD) patients' brains contain collagens and are embedded extracellularly. Several collagens have been proposed to influence Aβ aggregate formation, yet their role in clearance is unknown. To ... ...

    Abstract The amyloid beta (Aβ) plaques found in Alzheimer's disease (AD) patients' brains contain collagens and are embedded extracellularly. Several collagens have been proposed to influence Aβ aggregate formation, yet their role in clearance is unknown. To investigate the potential role of collagens in forming and clearance of extracellular aggregates in vivo, we created a transgenic
    MeSH term(s) Animals ; Humans ; Amyloid beta-Peptides ; Caenorhabditis elegans ; Peptide Hydrolases ; Disintegrins ; Alzheimer Disease ; Endopeptidases ; Plaque, Amyloid ; Metalloproteases/genetics ; Membrane Proteins ; ADAM Proteins
    Chemical Substances Amyloid beta-Peptides ; Peptide Hydrolases (EC 3.4.-) ; Disintegrins ; Endopeptidases (EC 3.4.-) ; Metalloproteases (EC 3.4.-) ; ADAM9 protein, human (EC 3.4.24.-) ; Membrane Proteins ; ADAM Proteins (EC 3.4.24.-)
    Language English
    Publishing date 2023-09-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.83465
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: End-of-life targeted degradation of DAF-2 insulin/IGF-1 receptor promotes longevity free from growth-related pathologies.

    Venz, Richard / Pekec, Tina / Katic, Iskra / Ciosk, Rafal / Ewald, Collin Yvès

    eLife

    2021  Volume 10

    Abstract: Preferably, lifespan-extending therapies should work when applied late in life without causing undesired pathologies. Reducing insulin/insulin-like growth factor (IGF)-1 signaling (IIS) increases lifespan across species, but the effects of reduced IIS ... ...

    Abstract Preferably, lifespan-extending therapies should work when applied late in life without causing undesired pathologies. Reducing insulin/insulin-like growth factor (IGF)-1 signaling (IIS) increases lifespan across species, but the effects of reduced IIS interventions in extreme geriatric ages remains unknown. Using the nematode
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Longevity/genetics ; Mutation ; Phenotype ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/genetics ; Receptor, Insulin/metabolism ; Signal Transduction/genetics
    Chemical Substances Caenorhabditis elegans Proteins ; DAF-2 protein, C elegans (EC 2.7.10.1) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1)
    Language English
    Publishing date 2021-09-10
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.71335
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article: Oxidative Stress Assays (arsenite and tBHP) in

    Ewald, Collin Yvès / Hourihan, John M / Blackwell, T Keith

    Bio-protocol

    2018  Volume 7, Issue 13

    Abstract: Cells and organisms face constant exposure to reactive oxygen species (ROS), either from the environment or as a by-product from internal metabolic processes. To prevent cellular damage from ROS, cells have evolved detoxification mechanisms. The ... ...

    Abstract Cells and organisms face constant exposure to reactive oxygen species (ROS), either from the environment or as a by-product from internal metabolic processes. To prevent cellular damage from ROS, cells have evolved detoxification mechanisms. The activation of these detoxification mechanisms and their downstream responses represent an overlapping defense response that can be tailored to different sources of ROS to adequately adapt and protect cells. In this protocol, we describe how to measure the sensitivity to oxidative stress from two different sources, arsenite and tBHP, using the nematode
    Language English
    Publishing date 2018-02-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.2365
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: Untangling Longevity, Dauer, and Healthspan in Caenorhabditis elegans Insulin/IGF-1-Signalling.

    Ewald, Collin Yvès / Castillo-Quan, Jorge Iván / Blackwell, T Keith

    Gerontology

    2017  Volume 64, Issue 1, Page(s) 96–104

    Abstract: The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other ... ...

    Abstract The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other genes in this pathway can double lifespan. Subsequent work has revealed that reduced IIS (rIIS) extends lifespan across diverse species, possibly including humans. In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism. Considerable progress has been made uncovering mechanisms that are affected by C. elegans rIIS. However, from the beginning it has remained unclear to what extent rIIS extends C. elegans lifespan by mobilizing dauer-associated mechanisms in adults. As we discuss, recent work has shed light on this question by determining that rIIS can extend C. elegans lifespan comparably through downstream processes that are either dauer-related or -independent. Importantly, these two lifespan extension programs can be distinguished genetically. It will now be critical to tease apart these programs, because each may involve different longevity-promoting mechanisms that may be relevant to higher organisms. A recent analysis of organismal "healthspan" has questioned the value of C. elegans rIIS as a paradigm for understanding healthy aging, as opposed to simply extending life. We discuss other work that argues strongly that C. elegans rIIS is indeed an invaluable model and consider the likely possibility that dauer-related processes affect parameters associated with health under rIIS conditions. Together, these studies indicate that C. elegans and analyses of rIIS in this organism will continue to provide unexpected and exciting results, and new paradigms that will be valuable for understanding healthy aging in humans.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/physiology ; Diapause/genetics ; Diapause/physiology ; Insulin/genetics ; Insulin/physiology ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/physiology ; Longevity/genetics ; Longevity/physiology ; Models, Biological ; Mutation ; Receptor, Insulin/genetics ; Receptor, Insulin/physiology ; Signal Transduction
    Chemical Substances Caenorhabditis elegans Proteins ; Insulin ; Insulin-Like Growth Factor I (67763-96-6) ; DAF-2 protein, C elegans (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1)
    Language English
    Publishing date 2017-09-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000480504
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article: Untangling Longevity, Dauer, and Healthspan in ; Insulin/IGF-1-Signalling

    Ewald, Collin Yvès / Castillo-Quan, Jorge Iván / Blackwell, T. Keith

    Gerontology

    2017  Volume 64, Issue 1, Page(s) 96–104

    Abstract: The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other ... ...

    Institution Eidgenössische Technische Hochschule (ETH) Zürich, Health Sciences and Technology, Schwerzenbach, Switzerland Department of Genetics, Harvard Medical School Harvard Stem Cell Institute, and Joslin Diabetes Center, Research Division, Boston, MA, USA
    Abstract The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other genes in this pathway can double lifespan. Subsequent work has revealed that reduced IIS (rIIS) extends lifespan across diverse species, possibly including humans. In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism. Considerable progress has been made uncovering mechanisms that are affected by C. elegans rIIS. However, from the beginning it has remained unclear to what extent rIIS extends C. elegans lifespan by mobilizing dauer-associated mechanisms in adults. As we discuss, recent work has shed light on this question by determining that rIIS can extend C. elegans lifespan comparably through downstream processes that are either dauer-related or -independent. Importantly, these two lifespan extension programs can be distinguished genetically. It will now be critical to tease apart these programs, because each may involve different longevity-promoting mechanisms that may be relevant to higher organisms. A recent analysis of organismal “healthspan” has questioned the value of C. elegans rIIS as a paradigm for understanding healthy aging, as opposed to simply extending life. We discuss other work that argues strongly that C. elegans rIIS is indeed an invaluable model and consider the likely possibility that dauer-related processes affect parameters associated with health under rIIS conditions. Together, these studies indicate that C. elegans and analyses of rIIS in this organism will continue to provide unexpected and exciting results, and new paradigms that will be valuable for understanding healthy aging in humans.
    Keywords Aging ; Dauer ; Insulin/IGF-1 signaling ; Longevity
    Language English
    Publishing date 2017-09-22
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Regenerative and Technological Section / Viewpoint
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000480504
    Database Karger publisher's database

    More links

    Kategorien

  7. Article ; Online: NADPH oxidase-mediated redox signaling promotes oxidative stress resistance and longevity through

    Ewald, Collin Yvès / Hourihan, John M / Bland, Monet S / Obieglo, Carolin / Katic, Iskra / Moronetti Mazzeo, Lorenza E / Alcedo, Joy / Blackwell, T Keith / Hynes, Nancy E

    eLife

    2017  Volume 6

    Abstract: Transient increases in mitochondrially-derived reactive oxygen species (ROS) activate an adaptive stress response to promote longevity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce ROS locally in response to various stimuli, and ... ...

    Abstract Transient increases in mitochondrially-derived reactive oxygen species (ROS) activate an adaptive stress response to promote longevity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce ROS locally in response to various stimuli, and thereby regulate many cellular processes, but their role in aging remains unexplored. Here, we identified the
    MeSH term(s) Animals ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/antagonists & inhibitors ; Caenorhabditis elegans Proteins/metabolism ; Longevity ; Nonheme Iron Proteins/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Oxidoreductases/antagonists & inhibitors ; Signal Transduction
    Chemical Substances Caenorhabditis elegans Proteins ; Nonheme Iron Proteins ; memo-1 protein, C elegans ; Bli-3 protein, C elegans (EC 1.-) ; Oxidoreductases (EC 1.-)
    Language English
    Publishing date 2017-01-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.19493
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top