Evidence map›Paper›PMID 37586578›Full record

ReviewNeuroscience and biobehavioral reviews2023

The impact of life stress on hallmarks of aging and accelerated senescence: Connections in sickness and in health.

Carey E Lyons, Maria Razzoli, Alessandro Bartolomucci

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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  19. Impact of night shift work on telomere length and epigenetic age in older workers.Journal of occupational medicine and toxicology (London, England) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Carey E LyonsDepartment of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, USA; Graduate Program in Neuroscience, University of Minnesota, Minneapolis, MN, USA.
Maria RazzoliDepartment of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, USA.
Alessandro BartolomucciDepartment of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, USA; Department of Medicine and Surgery, University of Parma, Parma, Italy. Electronic address: abartolo@umn.edu.
University of Minnesota · USUniversity of Parma · IT

Funding

Research Network on Animal Models to Understand Social Dimensions of AgingR24AG065172 · NIA · UNIVERSITY OF MINNESOTA · PI Susan C. Alberts, Alessandro Bartolomucci · 2020 to 2026
$2.6M
Mouse models for the influence of the social environment on health and agingR61AG078520 · NIA · UNIVERSITY OF MINNESOTA · PI BARTOLOMUCCI, ALESSANDRO · 2022 to 2023
$619k
NIA NIH HHS R24 AG065172NIA NIH HHS R61 AG078520
6 · The paper itself

Abstract

Chronic stress is a risk factor for numerous aging-related diseases and has been shown to shorten lifespan in humans and other social mammals. Yet how life stress causes such a vast range of diseases is still largely unclear. In recent years, the impact of stress on health and aging has been increasingly associated with the dysregulation of the so-called hallmarks of aging. These are basic biological mechanisms that influence intrinsic cellular functions and whose alteration can lead to accelerated aging. Here, we review correlational and experimental literature (primarily focusing on evidence from humans and murine models) on the contribution of life stress - particularly stress derived from adverse social environments - to trigger hallmarks of aging, including cellular senescence, sterile inflammation, telomere shortening, production of reactive oxygen species, DNA damage, and epigenetic changes. We also evaluate the validity of stress-induced senescence and accelerated aging as an etiopathological proposition. Finally, we highlight current gaps of knowledge and future directions for the field, and discuss perspectives for translational geroscience.

Indexed as

AgingCellular SenescenceAnimalsEpigenesis, GeneticHumansMammalsMiceStress, PsychologicalTelomere ShorteningBiological ageChronic stressEpigeneticGeroscienceSenescenceSocial stress

Identifiers

PMID37586578
PMCPMC10592082
OpenAlexW4385804383

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.