Evidence map›Paper›PMID 34278746›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2021

Reduced Acrolein Detoxification in akr1a1a Zebrafish Mutants Causes Impaired Insulin Receptor Signaling and Microvascular Alterations.

Haozhe Qi, Felix Schmöhl, Xiaogang Li, Xin Qian, Christoph T Tabler, Katrin Bennewitz, Carsten Sticht, Jakob Morgenstern, Thomas Fleming, Nadine Volk and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Effects of carnosine on the embryonic development and TiOFrontiers in veterinary science · 2023
    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

15 authors at 1 institution in 2 countries.

Haozhe QiDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Felix SchmöhlDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Xiaogang LiDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Xin QianDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Christoph T TablerDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Katrin BennewitzDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Carsten StichtNGS Core Facility, Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.
Jakob MorgensternDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, 69120, Germany.
Thomas FlemingDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, 69120, Germany.
Nadine VolkTissue Bank of the National Center for Tumor Diseases (NCT) Heidelberg, Heidelberg University, Heidelberg, 69120, Germany.
Ingrid HausserInstitute of Pathology IPH, EM Lab, Heidelberg University Hospital, Heidelberg, 69120, Germany.
Elena HeidenreichMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, Heidelberg, 69120, Germany.
Rüdiger HellMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, Heidelberg, 69120, Germany.
Peter Paul NawrothDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, 69120, Germany.
Jens KrollDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, 68167, Germany.ORCID 0000-0003-0908-2156
Heidelberg University · DE

Funding

China Scholarship Council CSC 201806230275Deutsche Forschungsgemeinschaft CRC1118Deutsche Forschungsgemeinschaft IRTG1874/2 DIAMICOMNational Natural Science Foundation of China 81800390
6 · The paper itself

Abstract

Increased acrolein (ACR), a toxic metabolite derived from energy consumption, is associated with diabetes and its complications. However, the molecular mechanisms are mostly unknown, and a suitable animal model with internal increased ACR does not exist for in vivo studying so far. Several enzyme systems are responsible for acrolein detoxification, such as Aldehyde Dehydrogenase (ALDH), Aldo-Keto Reductase (AKR), and Glutathione S-Transferase (GST). To evaluate the function of ACR in glucose homeostasis and diabetes, akr1a1a

Indexed as

AcroleinAnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalGlucoseHomeostasisLarvaLiverMetabolomicsReceptor, InsulinSignal TransductionTranscriptomeZebrafishAcroleinGlucoseReceptor, InsulinAcrolein (ACR)diabetesimpaired glucose homeostasisorgan complicationszebrafish

Identifiers

PMID34278746
PMCPMC8456208
OpenAlexW3185632860

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.