Evidence map›Paper›PMID 38400874›Full record

ReviewGeroScience2024

Metabolic dysfunction and the development of physical frailty: an aging war of attrition.

William A Fountain, Taylor S Bopp, Michael Bene, Jeremy D Walston

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.5field-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

28 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Article
  11. Article
  12. Frailty Exacerbates Disability in Progressive Multiple Sclerosis.Annals of clinical and translational neurology · 2026
    Article
  13. Aging-Driven Inter-Organ Crosstalk in Postmenopausal Osteoporosis: From Immunometabolic Drift to Multisystem Frailty.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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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

4 authors at 1 institution in 1 country.

William A FountainDivision of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, 21224, USA.
Taylor S BoppDivision of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, 21224, USA.
Michael BeneDivision of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, 21224, USA.
Jeremy D WalstonDivision of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, 21224, USA. jwalston@jhmi.edu.ORCID 0000-0002-6965-2723
Johns Hopkins University · US

Funding

Technological Assessment and Solutions Core - RC4P30AG021334 · NIA · JOHNS HOPKINS UNIVERSITY · PI Jeremy D Walston · 2003 to 2026
$33.2M
Translational Aging Research Training ProgramT32AG058527 · NIA · JOHNS HOPKINS UNIVERSITY · PI Peter M. Abadir, Esther Seunghee Oh · 2018 to 2026
$4.0M
NIA NIH HHS P30 AG021334NIA NIH HHS T32 AG058527
6 · The paper itself

Abstract

The World Health Organization recently declared 2021-2030 the decade of healthy aging. Such emphasis on healthy aging requires an understanding of the biologic challenges aging populations face. Physical frailty is a syndrome of vulnerability that puts a subset of older adults at high risk for adverse health outcomes including functional and cognitive decline, falls, hospitalization, and mortality. The physiology driving physical frailty is complex with age-related biological changes, dysregulated stress response systems, chronic inflammatory pathway activation, and altered energy metabolism all likely contributing. Indeed, a series of recent studies suggests circulating metabolomic distinctions can be made between frail and non-frail older adults. For example, marked restrictions on glycolytic and mitochondrial energy production have been independently observed in frail older adults and collectively appear to yield a reliance on the highly fatigable ATP-phosphocreatine (PCr) energy system. Further, there is evidence that age-associated impairments in the primary ATP generating systems (glycolysis, TCA cycle, electron transport) yield cumulative deficits and fail to adequately support the ATP-PCr system. This in turn may acutely contribute to several major components of the physical frailty phenotype including muscular fatigue, weakness, slow walking speed and, over time, result in low physical activity and accelerate reductions in lean body mass. This review describes specific age-associated metabolic declines and how they can collectively lead to metabolic inflexibility, ATP-PCr reliance, and the development of physical frailty. Further investigation remains necessary to understand the etiology of age-associated metabolic deficits and develop targeted preventive strategies that maintain robust metabolic health in older adults.

Indexed as

AgingEnergy MetabolismFrailtyAgedFrail ElderlyHumansAgingEnergyFrailtyMetabolismSkeletal muscle

Identifiers

PMID38400874
PMCPMC11226579
OpenAlexW4392139418

What OpenQuestion holds

Textmetadata
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.