Evidence map›Paper›PMID 29335816›Full record

ReviewBiogerontology2018

Organ reserve, excess metabolic capacity, and aging.

Hani Atamna, Alfred Tenore, Forshing Lui, Joseph M Dhahbi

Abstract readReview
In one paragraph

Review in Biogerontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. International journal of molecular sciences · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Neurosteroids: a lifelong impact on brain health.Frontiers in behavioral neuroscience · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Towards early detection of neurodegenerative diseases: A gut feeling.Frontiers in cell and developmental biology · 2023
    Review
  17. Article
  18. Article
  19. Homeostatic medicine: a strategy for exploring health and disease.Current medicine (Cham, Switzerland) · 2022
    Review
  20. Review
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.

Hani AtamnaSchool of Medicine, California University of Science and Medicine (CUSM), 217 E Club Center Dr. Suite A, San Bernardino, CA, 92408, USA. atamnah@calmedu.org.
Alfred TenoreSchool of Medicine, California University of Science and Medicine (CUSM), 217 E Club Center Dr. Suite A, San Bernardino, CA, 92408, USA.
Forshing LuiSchool of Medicine, California University of Science and Medicine (CUSM), 217 E Club Center Dr. Suite A, San Bernardino, CA, 92408, USA.
Joseph M DhahbiSchool of Medicine, California University of Science and Medicine (CUSM), 217 E Club Center Dr. Suite A, San Bernardino, CA, 92408, USA.

Funding

Understanding the mechanism of cell senescence delay by methylene blueR15AG041414 · NIA · GEISINGER COMMONWEALTH SCHOOL OF MEDICINE · PI ATAMNA, HANI · 2011 to 2011
$314k
NIA NIH HHS R15 AG041414NIH HHS R15AG041414
6 · The paper itself

Abstract

"Organ reserve" refers to the ability of an organ to successfully return to its original physiological state following repeated episodes of stress. Clinical evidence shows that organ reserve correlates with the ability of older adults to cope with an added workload or stress, suggesting a role in the process of aging. Although organ reserve is well documented clinically, it is not clearly defined at the molecular level. Interestingly, several metabolic pathways exhibit excess metabolic capacities (e.g., bioenergetics pathway, antioxidants system, plasticity). These pathways comprise molecular components that have an excess of quantity and/or activity than that required for basic physiological demand in vivo (e.g., mitochondrial complex IV or glycolytic enzymes). We propose that the excess in mtDNA copy number and tandem DNA repeats of telomeres are additional examples of intrinsically embedded structural components that could comprise excess capacity. These excess capacities may grant intermediary metabolism the ability to instantly cope with, or manage, added workload or stress. Therefore, excess metabolic capacities could be viewed as an innate mechanism of adaptability that substantiates organ reserve and contributes to the cellular defense systems. If metabolic excess capacities or organ reserves are impaired or exhausted, the ability of the cell to cope with stress is reduced. Under these circumstances cell senescence, transformation, or death occurs. In this review, we discuss excess metabolic and structural capacities as integrated metabolic pathways in relation to organ reserve and cellular aging.

Indexed as

Adaptation, PhysiologicalAgingAnimalsDNA, MitochondrialElectron Transport Complex IVEnergy MetabolismGlycolysisHumansModels, BiologicalNeuronsPentose Phosphate PathwayTelomereTissue SurvivalDNA, MitochondrialElectron Transport Complex IVComplex IVExcess metabolic capacityMitochondriamtDNAOrgan reserveTelomeres

Identifiers

PMID29335816
PMCPMC5835208

What OpenQuestion holds

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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.