Evidence map›Paper›PMID 28696246›Full record

ArticleJournal of the American Society of Nephrology : JASN2017

Farnesoid X Receptor Agonism Protects against Diabetic Tubulopathy: Potential Add-On Therapy for Diabetic Nephropathy.

Andi Marquardt, Moh'd Mohanad Al-Dabet, Sanchita Ghosh, Shrey Kohli, Jayakumar Manoharan, Ahmed ElWakiel, Ihsan Gadi, Fabian Bock, Sumra Nazir, Hongjie Wang and 6 more

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 74 citations in OpenAlex.

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  17. Role of FXR in Renal Physiology and Kidney Diseases.International journal of molecular sciences · 2023
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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

16 authors at 5 institutions in 3 countries.

Andi MarquardtInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Moh'd Mohanad Al-DabetInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Sanchita GhoshInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Shrey KohliInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Jayakumar ManoharanInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Ahmed ElWakielInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Ihsan GadiInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Fabian BockInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Sumra NazirInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Hongjie WangInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Jonathan A LindquistClinic of Nephrology and Hypertension, Diabetes and Endocrinology, Otto-von-Guericke University, Magdeburg, Germany.
Peter Paul NawrothDepartment of Internal Medicine I and Clinical Chemistry, German Diabetes Center, University of Heidelberg, Heidelberg, Germany.
Thati MadhusudhanInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Peter R MertensClinic of Nephrology and Hypertension, Diabetes and Endocrinology, Otto-von-Guericke University, Magdeburg, Germany.
Khurrum ShahzadInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
Berend IsermannInstitute of Clinical Chemistry and Pathobiochemistry and berend.isermann@med.ovgu.de.
Otto-von-Guericke University Magdeburg · DEGerman Center for Diabetes Research · DEJohannes Gutenberg University Mainz · DETongji Hospital · CNUniversity of Sargodha · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Established therapies for diabetic nephropathy (dNP) delay but do not prevent its progression. The shortage of established therapies may reflect the inability to target the tubular compartment. The chemical chaperone tauroursodeoxycholic acid (TUDCA) ameliorates maladaptive endoplasmic reticulum (ER) stress signaling and experimental dNP. Additionally, TUDCA activates the farnesoid X receptor (FXR), which is highly expressed in tubular cells. We hypothesized that TUDCA ameliorates maladaptive ER signaling

Indexed as

Kidney TubulesAnimalsDiabetic NephropathiesHumansMaleMiceMice, Inbred C57BLReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTaurochenodeoxycholic AcidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTaurochenodeoxycholic AcidursodoxicoltaurineACE inhibitorsdiabetic nephropathyFXRtudca ER-stress diabetes

Identifiers

PMID28696246
PMCPMC5661274
OpenAlexW2736271984

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.