Evidence map›Paper›PMID 32899870›Full record

ReviewInternational journal of molecular sciences2020

p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?

Eyal Bengal, Sharon Aviram, Tony Hayek

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-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

52 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
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  3. [IOX1 alleviates hepatic ischemia-reperfusion injury by inhibiting mitogen-activated protein kinase signaling pathway].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
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  8. Biochemistry and biophysics reports · 2026
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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 2 institutions in 1 country.

Eyal BengalDepartment of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel.
Sharon AviramDepartment of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel.
Tony HayekDepartment of Internal Medicine E, Rambam Medical Center, Haifa 31096, Israel.
Technion – Israel Institute of Technology · ILRambam Health Care Campus · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein kinase (MAPK) is one of several signaling pathways that drive the metabolic adaptation of skeletal muscle to exercise. p38 MAPK also participates in the development of pathological traits resulting from excessive caloric intake and obesity that cause metabolic syndrome and type 2 diabetes (T2D). Whereas p38 MAPK increases insulin-independent glucose uptake and oxidative metabolism in muscles during exercise, it contrastingly mediates insulin resistance and glucose intolerance during metabolic syndrome development. This article provides an overview of the apparent contradicting roles of p38 MAPK in the adaptation of skeletal muscles to exercise and to pathological conditions leading to glucose intolerance and T2D. Here, we focus on the involvement of p38 MAPK in glucose metabolism of skeletal muscle, and discuss the possibility of targeting this pathway to prevent the development of T2D.

Indexed as

AnimalsBiological TransportCarbohydrate MetabolismDiabetes Mellitus, Type 2ExerciseGlucoseGlucose IntoleranceHumansInsulinInsulin ResistanceMuscle, SkeletalObesityp38 Mitogen-Activated Protein KinasesPhosphorylationSignal TransductionGlucoseInsulinp38 Mitogen-Activated Protein Kinasesenergy metabolismexercisep38 MAPKsignal transductionskeletal muscletype 2 diabetes

Identifiers

PMID32899870
PMCPMC7555282
OpenAlexW3083229866

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.