Evidence map›Paper›PMID 23356266›Full record

ReviewBiochemical Society transactions2013

Metabolic triad in brain aging: mitochondria, insulin/IGF-1 signalling and JNK signalling.

Fei Yin, Tianyi Jiang, Enrique Cadenas

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Review
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  12. Dysregulation of IGF-1/GLP-1 signaling in the progression of ALS: potential target activators and influences on neurological dysfunctions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  13. Review
  14. Inhibition ofAging · 2019
    Article
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  16. Article
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  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

3 authors at 1 institution in 1 country.

Fei YinPharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA 90089, USA.
Tianyi Jiang
Enrique Cadenas
University of Southern California · US

Funding

Timing of Menopausal Hormone Therapy across Perimenopause to Menopause Transition: Neuroimmune System in BrainP01AG026572 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Schantel Williams · 2006 to 2026
$53.7M
OXIDATIVE STRESS, MITOCHONDRIAL DYSFUNCTION, AND AGINGR01AG016718 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CADENAS, ENRIQUE · 1999 to 2009
$2.5M
NIA NIH HHS P01 AG026572NIA NIH HHS P01AG026572NIA NIH HHS R01 AG016718NIA NIH HHS R01AG016718
6 · The paper itself

Abstract

Mitochondria generate second messengers, such as H2O2, that are involved in the redox regulation of cell signalling and their function is regulated by several cytosolic signalling pathways. IIS [insulin/IGF1 (insulin-like growth factor 1) signalling] in the brain proceeds mainly through the PI3K (phosphatidylinositol 3-kinase)-Akt (protein kinase B) pathway, which is involved in the regulation of synaptic plasticity and neuronal survival via the maintenance of the bioenergetic and metabolic capacities of mitochondria. Conversely, the JNK (c-Jun N-terminal kinase) pathway is induced by increased oxidative stress and JNK translocation to the mitochondrion results in impairment of energy metabolism. Moreover, IIS and JNK signalling interact with and antagonize each other. This review focuses on functional outcomes of a metabolic triad that entails the co-ordination of mitochondrial function (energy transducing and redox regulation), IIS and JNK signalling, in the aging brain and in neurodegenerative disorders, such as Alzheimer's disease.

Indexed as

Signal TransductionAgingBrainDisease ProgressionHumansInsulinInsulin-Like Growth Factor IMAP Kinase Kinase 4MitochondriaNeurodegenerative DiseasesInsulinInsulin-Like Growth Factor IMAP Kinase Kinase 4

Identifiers

PMID23356266
PMCPMC9934302
OpenAlexW2038683700

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.