Evidence map›Paper›PMID 24663223›Full record

ReviewNature reviews. Endocrinology2014

Mitochondrial allostatic load puts the 'gluc' back in glucocorticoids.

Martin Picard, Robert-Paul Juster, Bruce S McEwen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 4 pooled it
14.2field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 4 syntheses or guidelines pooled it, 385 citations in OpenAlex.

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  6. Neurobiological and Anti-Inflammatory Effects of a Deep Diaphragmatic Breathing Technique Based on Neofunctional Psychotherapy: A Pilot RCT.Stress and health : journal of the International Society for the Investigation of Stress · 2024
    Trial
  7. Exploring cannabidiol effects on inflammatory markers in individuals with cocaine use disorder: a randomized controlled trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Trial
  8. Circulating cell-free mitochondrial DNA, but not leukocyte mitochondrial DNA copy number, is elevated in major depressive disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Trial
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137 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Martin PicardCenter for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia and the University of Pennsylvania, 3501 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Robert-Paul JusterIntegrated Program in Neuroscience, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC H3A 2B4, Canada.
Bruce S McEwenHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Children's Hospital of Philadelphia · USMontreal Neurological Institute and Hospital · CARockefeller University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The link between chronic psychosocial and metabolic stress and the pathogenesis of disease has been extensively documented. Nevertheless, the cellular mechanisms by which stressful life experiences and their associated primary neuroendocrine mediators cause biological damage and increase disease risk remain poorly understood. The allostatic load model of chronic stress focuses on glucocorticoid dysregulation. In this Perspectives, we expand upon the metabolic aspects of this model-particularly glucose imbalance-and propose that mitochondrial dysfunction constitutes an early, modifiable target of chronic stress and stress-related health behaviours. Central to this process is mitochondrial regulation of energy metabolism and cellular signalling. Chronically elevated glucose levels damage both mitochondria and mitochondrial DNA, generating toxic products that can promote systemic inflammation, alter gene expression and hasten cell ageing. Consequently, the concept of 'mitochondrial allostatic load' defines the deleterious structural and functional changes that mitochondria undergo in response to elevated glucose levels and stress-related pathophysiology.

Indexed as

AgingAllostasisAnimalsCellular SenescenceDNA, MitochondrialGlucocorticoidsGlucoseHealthHumansMitochondriaStress, PhysiologicalStress, PsychologicalDNA, MitochondrialGlucocorticoidsGlucose

Identifiers

PMID24663223
OpenAlexW1974323299

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.