Biological age is increased by stress and restored upon recovery.

aging biological age dynamics epigenetic aging clocks recovery stress

Journal

Cell metabolism
ISSN: 1932-7420
Titre abrégé: Cell Metab
Pays: United States
ID NLM: 101233170

Informations de publication

Date de publication:
02 05 2023
Historique:
received: 07 06 2022
revised: 22 12 2022
accepted: 20 03 2023
medline: 5 5 2023
pubmed: 23 4 2023
entrez: 22 04 2023
Statut: ppublish

Résumé

Aging is classically conceptualized as an ever-increasing trajectory of damage accumulation and loss of function, leading to increases in morbidity and mortality. However, recent in vitro studies have raised the possibility of age reversal. Here, we report that biological age is fluid and exhibits rapid changes in both directions. At epigenetic, transcriptomic, and metabolomic levels, we find that the biological age of young mice is increased by heterochronic parabiosis and restored following surgical detachment. We also identify transient changes in biological age during major surgery, pregnancy, and severe COVID-19 in humans and/or mice. Together, these data show that biological age undergoes a rapid increase in response to diverse forms of stress, which is reversed following recovery from stress. Our study uncovers a new layer of aging dynamics that should be considered in future studies. The elevation of biological age by stress may be a quantifiable and actionable target for future interventions.

Identifiants

pubmed: 37086720
pii: S1550-4131(23)00093-1
doi: 10.1016/j.cmet.2023.03.015
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

807-820.e5

Subventions

Organisme : NIA NIH HHS
ID : R21 AG065943
Pays : United States
Organisme : NIBIB NIH HHS
ID : T32 EB016652
Pays : United States

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Jesse R Poganik (JR)

Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Bohan Zhang (B)

Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Gurpreet S Baht (GS)

Department of Orthopaedic Surgery, Duke University, Durham, NC 27701, USA; Duke Molecular Physiology Institute, Duke University, Durham, NC 27701, USA.

Alexander Tyshkovskiy (A)

Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Amy Deik (A)

Broad Institute of MIT and Harvard, Cambridge, MA 01241, USA.

Csaba Kerepesi (C)

Institute for Computer Science and Control (SZTAKI), Eötvös Loránd Research Network, Budapest, 1111, Hungary.

Sun Hee Yim (SH)

Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Ake T Lu (AT)

Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Altos Labs, San Diego, CA, USA.

Amin Haghani (A)

Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Altos Labs, San Diego, CA, USA.

Tong Gong (T)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Anna M Hedman (AM)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Ellika Andolf (E)

Department of Clinical Sciences, Division of Obstetrics and Gynaecology, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.

Göran Pershagen (G)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Centre for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden.

Catarina Almqvist (C)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.

Clary B Clish (CB)

Broad Institute of MIT and Harvard, Cambridge, MA 01241, USA.

Steve Horvath (S)

Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Altos Labs, San Diego, CA, USA; Department of Biostatistics, School of Public Health, University of California, Los Angeles, Los Angeles, CA 90095, USA.

James P White (JP)

Duke Molecular Physiology Institute, Duke University, Durham, NC 27701, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27701, USA. Electronic address: james.white@duke.edu.

Vadim N Gladyshev (VN)

Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 01241, USA. Electronic address: vgladyshev@rics.bwh.harvard.edu.

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Classifications MeSH