Evidence map›Paper›PMID 30361814›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2018

Hypoxia-inducible factor 1α protects peripheral sensory neurons from diabetic peripheral neuropathy by suppressing accumulation of reactive oxygen species.

Daniel Rangel Rojas, Irmgard Tegeder, Rohini Kuner, Nitin Agarwal

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 65 citations in OpenAlex.

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  16. HIF‑1α in cerebral ischemia (Review).Molecular medicine reports · 2022
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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

4 authors at 2 institutions in 1 country.

Daniel Rangel RojasInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, D-69120, Heidelberg, Germany.
Irmgard TegederInstitute for Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany.
Rohini KunerInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, D-69120, Heidelberg, Germany.
Nitin AgarwalInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, D-69120, Heidelberg, Germany. nitin.agarwal@pharma.uni-heidelberg.de.
Heidelberg University · DEGoethe University Frankfurt · DE

Funding

Deutsche Forschungsgemeinschaft CRC 1118 project B06Deutsche Forschungsgemeinschaft CRC 1118, Project B06
6 · The paper itself

Abstract

Diabetic peripheral neuropathy (DPN) is one of the most common diabetic complications. Mechanisms underlying nerve damage and sensory loss following metabolic dysfunction remain largely unclear. Recently, hyperglycemia-induced mitochondrial dysfunction and the generation of reactive oxygen species (ROS) have gained attention as possible mechanisms of organ damage in diabetes. Hypoxia-inducible factor 1 (HIF1α) is a key transcription factor activated by hypoxia, hyperglycemia, nitric oxide as well as ROS, suggesting a fundamental role in DPN susceptibility. We analyzed regulation of HIF1α in response to prolonged hyperglycemia. Genetically modified mutant mice, which conditionally lack HIF1α in peripheral sensory neurons (SNS-HIF1α

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NeuropathiesFemaleHypoxia-Inducible Factor 1, alpha SubunitMaleMice, TransgenicReactive Oxygen SpeciesSensory Receptor CellsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReactive Oxygen SpeciesDPNHyperglycemiaROSSensory neuronsStreptozotocin

Identifiers

PMID30361814
OpenAlexW2963982415

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.