Evidence map›Paper›PMID 27527620›Full record

ReviewClinical and translational medicine2016

Creatine kinase in ischemic and inflammatory disorders.

David Kitzenberg, Sean P Colgan, Louise E Glover

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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  17. Myocardial Disorders in BDNF-Deficient Rats: Limited Recovery Post-Moderate Endurance Training.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
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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.

David KitzenbergMucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, 12700 East 19th Ave. MS B-146, Aurora, CO, 80045, USA.
Sean P ColganMucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, 12700 East 19th Ave. MS B-146, Aurora, CO, 80045, USA.
Louise E GloverMucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, 12700 East 19th Ave. MS B-146, Aurora, CO, 80045, USA. louise.glover@ucdenver.edu.ORCID http://orcid.org/0000-0001-9056-1810
University of Colorado Anschutz Medical Campus · US

Funding

Mechanisms of Adenosine ProtectionR01DK095491 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Sean P Colgan · 2012 to 2026
$4.9M
Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
METABOLIC CONTROL OF EPITHELIAL AUTOPHAGY DURING INFLAMMATIONR01DK103712 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2015 to 2019
$1.7M
Metabolic Regulation of Mucosal InflammationI01BX002182 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI COLGAN, SEAN P · 2014 to 2025
–
BLRD VA I01 BX002182NIDDK NIH HHS R01 DK095491NIDDK NIH HHS R01 DK103712NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

The creatine/phosphocreatine pathway plays a conserved and central role in energy metabolism. Compartmentalization of specific creatine kinase enzymes permits buffering of local high energy phosphates in a thermodynamically favorable manner, enabling both rapid energy storage and energy transfer within the cell. Augmentation of this metabolic pathway by nutritional creatine supplementation has been shown to elicit beneficial effects in a number of diverse pathologies, particularly those that incur tissue ischemia, hypoxia or oxidative stress. In these settings, creatine and phosphocreatine prevent depletion of intracellular ATP and internal acidification, enhance post-ischemic recovery of protein synthesis and promote free radical scavenging and stabilization of cellular membranes. The creatine kinase energy system is itself further regulated by hypoxic signaling, highlighting the existence of endogenous mechanisms in mammals that can enhance creatine metabolism during oxygen deprivation to promote tissue resolution and homeostasis. Here, we review recent insights into the creatine kinase pathway, and provide rationale for dietary creatine supplementation in human ischemic and inflammatory pathologies.

Indexed as

CreatineCreatine kinaseEnergeticsHypoxiaIschemiaMetabolismMitochondriaPhosphocreatine

Identifiers

PMID27527620
PMCPMC4987751
OpenAlexW2512146915

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.