Evidence map›Paper›PMID 27321753›Full record

ReviewProgress in neurobiology2017

Mitochondrial function in hypoxic ischemic injury and influence of aging.

P Benson Ham, Raghavan Raju

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 5 pooled it
15.0field-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

220 citing papers in PubMed, 5 syntheses or guidelines pooled it, 355 citations in OpenAlex.

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  11. The Pathogenesis of Preeclampsia: Hypoxia and the Unfolded Protein Response.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  12. [Research progress on the roles of mitochondrial fusion, fission, and mitophagy in burn wound healing​].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
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160 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

2 authors at 1 institution in 1 country.

P Benson HamDepartment of Surgery, Georgia Regents University, Augusta, GA, United States.
Raghavan RajuDepartment of Surgery, Georgia Regents University, Augusta, GA, United States; Department of Laboratory Sciences, Georgia Regents University, Augusta, GA, United States; Department of Biochemistry and Molecular Biology, Georgia Regents University, Augusta, GA, United States. Electronic address: RRaju@augusta.edu.
Georgia Regents Medical Center · US

Funding

Resveratrol as an adjunct to resuscitation fluid following hemorrhage injuryR01GM101927 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAJU, RAGHAVAN PILLAI · 2012 to 2016
$1.1M
NIGMS NIH HHS R01 GM101927
6 · The paper itself

Abstract

Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

Indexed as

AgingAnimalsHumansHypoxiaIschemiaMitochondriaAlzheimer’s diseaseApoptosisAutophagyBlood brain barrierHypoxiaIntermitochondrial signal propagationIschemia/reperfusionMitokineMitoquinoneNuclear-mitochondria cross-talkOxidative phosphorylationParkinson’s diseasePseudohypoxiaResveratrol, SIRT1, sirtuinsStroke, myocardial infarctionTempolTunneling nanotube

Identifiers

PMID27321753
PMCPMC5161736
OpenAlexW2436474716

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.