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      New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary

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          Abstract

          Genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, loss of proteostasis, deregulated nutrient-sensing, cellular senescence, stem cell exhaustion, and altered intercellular communication were the original nine hallmarks of ageing proposed by López-Otín and colleagues in 2013. The proposal of these hallmarks of ageing has been instrumental in guiding and pushing forward research on the biology of ageing. In the nearly past 10 years, our in-depth exploration on ageing research has enabled us to formulate new hallmarks of ageing which are compromised autophagy, microbiome disturbance, altered mechanical properties, splicing dysregulation, and inflammation, among other emerging ones. Amalgamation of the ‘old’ and ‘new’ hallmarks of ageing may provide a more comprehensive explanation of ageing and age-related diseases, shedding light on interventional and therapeutic studies to achieve healthy, happy, and productive lives in the elderly.

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          The Hallmarks of Aging

          Carlos López-Otín, Maria Blasco, Linda Partridge … (2014)
          Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty

            Luigi Ferrucci, Elisa Fabbri (2018)
            Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty - which affect clinical manifestations, prognosis, and response to treatment - and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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              Inflammaging: a new immune–metabolic viewpoint for age-related diseases

              Paolo Parini, Aurelia Santoro, Cristina Giuliani … (2018)
              Ageing and age-related diseases share some basic mechanistic pillars that largely converge on inflammation. During ageing, chronic, sterile, low-grade inflammation - called inflammaging - develops, which contributes to the pathogenesis of age-related diseases. From an evolutionary perspective, a variety of stimuli sustain inflammaging, including pathogens (non-self), endogenous cell debris and misplaced molecules (self) and nutrients and gut microbiota (quasi-self). A limited number of receptors, whose degeneracy allows them to recognize many signals and to activate the innate immune responses, sense these stimuli. In this situation, metaflammation (the metabolic inflammation accompanying metabolic diseases) is thought to be the form of chronic inflammation that is driven by nutrient excess or overnutrition; metaflammation is characterized by the same mechanisms underpinning inflammaging. The gut microbiota has a central role in both metaflammation and inflammaging owing to its ability to release inflammatory products, contribute to circadian rhythms and crosstalk with other organs and systems. We argue that chronic diseases are not only the result of ageing and inflammaging; these diseases also accelerate the ageing process and can be considered a manifestation of accelerated ageing. Finally, we propose the use of new biomarkers (DNA methylation, glycomics, metabolomics and lipidomics) that are capable of assessing biological versus chronological age in metabolic diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aging (Albany NY)
                Journal ID (publisher-id): Aging
                Title: Aging (Albany NY)
                Publisher: Impact Journals
                ISSN (Electronic): 1945-4589
                Publication date Collection: 31 August 2022
                Publication date (Electronic): 29 August 2022
                Volume: 14
                Issue: 16
                Pages: 6829-6839
                Affiliations
                [1 ]Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway
                [2 ]Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow 30-348, Poland
                [3 ]Center for Healthy Ageing, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen 2400, Denmark
                [4 ]Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital – Bispebjerg and Frederiksberg, Copenhagen 2400, Denmark
                [5 ]Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden
                [6 ]Stem Cell Laboratory, UCL Cancer Institute, University College London, London, UK
                [7 ]Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Glostrup 2600, Denmark
                [8 ]The David and Inez Myers Laboratory of Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Tel Aviv University School of Medicine P.O.B 39040, Tel Aviv, Israel
                [9 ]Department of Environmental and Occupational Health, University of Pittsburgh School of Public Health, Pittsburgh, PA 15261, USA
                [10 ]Department of Functional Genomics and Cancer, IGBMC, CNRS/INSERM/University of Strasbourg, Equipe labellisée Ligue contre le Cancer, Strasbourg, France
                [11 ]College of Medicine, Center for Genomics and Precision Medicine, National Taiwan University, Taipei City, Taiwan
                [12 ]UK National Innovation Centre for Ageing, The Catalyst, 3 Science Square, Newcastle University, Newcastle upon Tyne, NE4 5TG, UK
                [13 ]Buck Institute for Research on Ageing, Novato, CA 94945, USA
                [14 ]Section on DNA Repair, National Institute on Ageing, Baltimore, MD 21224, USA
                [15 ]Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK
                [16 ]Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000, Denmark
                [17 ]The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway
                [18 ]UPMC Hillman Cancer Center, Pittsburgh, PA 15232, USA
                Author notes
                [*]

                Equal contribution

                Correspondence to: Tinna Stevnsner; email: tvs@mbg.au.dk
                Correspondence to: Lene Juel Rasmussen; email: lenera@sund.ku.dk
                Correspondence to: Evandro F. Fang; email: e.f.fang@medisin.uio.no
                Article
                Publisher ID: 204248 Publisher ID: 204248
                DOI: 10.18632/aging.204248
                PMC ID: 9467401
                PubMed ID: 36040386
                SO-VID: 085d3629-8485-40d9-837e-f8feebd3665a
                Copyright © Copyright: © 2022 Schmauck-Medina et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 30 July 2022
                Date accepted : 14 August 2022
                Categories
                Subject: Review

                ScienceOpen disciplines: Cell biology
                Keywords: hallmarks of ageing,neurodegeneration,healthspan,longevity,autophagy
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: hallmarks of ageing, neurodegeneration, healthspan, longevity, autophagy

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