Evidence map›Paper›PMID 35179657›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2022

Elevated level of lysophosphatidic acid among patients with HNF1B mutations and its role in RCAD syndrome: a multiomic study.

Beata Małachowska, Justyna Janikiewicz, Karolina Pietrowska, Krystyna Wyka, Joanna Madzio, Kamila Wypyszczak, Marcin Tkaczyk, Sławomir Chrul, Rafał Zwiech, Anna Hogendorf and 7 more

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

Article in Metabolomics : Official journal of the Metabolomic Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
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

17 authors at 6 institutions in 2 countries.

Beata MałachowskaDepartment of Biostatistics and Translational Medicine, Medical University of Lodz, 15 Mazowiecka Street, 92-215, Lodz, Poland.ORCID http://orcid.org/0000-0003-4009-8797
Justyna JanikiewiczLaboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology PAS, 3 Pasteur Street, 02-093, Warsaw, Poland.
Karolina PietrowskaClinical Research Centre, Medical University of Bialystok, 24a Sklodowska-Curie Street, 15-276, Bialystok, Poland.ORCID http://orcid.org/0000-0002-6639-2823
Krystyna WykaDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, 36/50 Sporna Street, 91-738, Lodz, Poland.
Joanna MadzioDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, 36/50 Sporna Street, 91-738, Lodz, Poland.
Kamila WypyszczakDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, 36/50 Sporna Street, 91-738, Lodz, Poland.
Marcin TkaczykDepartment of Pediatrics, Immunology and Nephrology, Polish Mother's Memorial Hospital Research Institute, 281/289 Rzgowska Street, 93-338, Lodz, Poland.
Sławomir ChrulDepartment of Pediatrics, Immunology and Nephrology, Polish Mother's Memorial Hospital Research Institute, 281/289 Rzgowska Street, 93-338, Lodz, Poland.
Rafał ZwiechDepartment of Kidney Transplantation/Dialysis Department, Barlicki Memorial Teaching Hospital No. 1, Medical University of Lodz, 22 Kopcinskiego Street, 90-153, Lodz, Poland.
Anna HogendorfDepartment of Pediatrics, Diabetology, Endocrinology, and Nephrology, Medical University of Lodz, 36/50 Sporna Street, 91-738, Lodz, Poland.
Maciej T MałeckiDepartment of Metabolic Diseases, Medical College, Jagiellonian University, 2 Jakubowskiego Street, 30-688, Cracov, Poland.
Maciej BorowiecDepartment of Clinical Genetics, Medical University of Lodz, 251 Pomorska Street, 92-213, Lodz, Poland.
Adam KrętowskiClinical Research Centre, Medical University of Bialystok, 24a Sklodowska-Curie Street, 15-276, Bialystok, Poland.ORCID http://orcid.org/0000-0002-4522-4978
Wojciech MłynarskiDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, 36/50 Sporna Street, 91-738, Lodz, Poland.
Agnieszka DobrzyńLaboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology PAS, 3 Pasteur Street, 02-093, Warsaw, Poland.
Michał CiborowskiClinical Research Centre, Medical University of Bialystok, 24a Sklodowska-Curie Street, 15-276, Bialystok, Poland.ORCID http://orcid.org/0000-0003-3729-0518
Wojciech FendlerDepartment of Biostatistics and Translational Medicine, Medical University of Lodz, 15 Mazowiecka Street, 92-215, Lodz, Poland. wojciech.fendler@umed.lodz.pl.ORCID http://orcid.org/0000-0002-5083-9168
Medical University of Lodz · PLMedical University of Białystok · PLInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLDana-Farber Cancer Institute · USJagiellonian University · PLPolish Mother’s Memorial Hospital Research Institute · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPatients with hepatocyte nuclear factor-1 beta (HNF1B) mutations present a variable phenotype with two main symptoms: maturity onset diabetes of the young (MODY) and polycystic kidney disease (PKD).

objectivesIdentification of serum metabolites specific for HNF1Bmut and evaluation of their role in disease pathogenesis.

methodsWe recruited patients with HNF1Bmut (N = 10), HNF1Amut (N = 10), PKD: non-dialyzed and dialyzed (N = 8 and N = 13); and healthy controls (N = 12). Serum fingerprinting was performed by LC-QTOF-MS. Selected metabolite was validated by ELISA (enzyme-linked immunosorbent assay) measurements and then biologically connected with HNF1B by in silico analysis. HepG2 were stimulated with lysophosphatidic acid (LPA) and HNF1B gene was knocked down (kd) by small interfering RNA. Transcriptomic analysis with microarrays and western blot measurements were performed.

resultsSerum levels of six metabolites including: arachidonic acid, hydroxyeicosatetraenoic acid, linoleamide and three LPA (18:1, 18:2 and 20:4), had AUC (the area under the curve) > 0.9 (HNF1Bmut vs comparative groups). The increased level of LPA was confirmed by ELISA measurements. In HepG2

conclusionsLPA is elevated in sera of patients with HNF1Bmut. LPA contributes to the pathogenesis of HNF1B-MODY by affecting Wnt/GSK-3 signaling.

Indexed as

Glycogen Synthase Kinase 3Kidney Diseases, CysticHepatocyte Nuclear Factor 1-betaHumansLysophospholipidsMetabolomicsMutationGlycogen Synthase Kinase 3Hepatocyte Nuclear Factor 1-betaHNF1B protein, humanlysophosphatidic acidLysophospholipidsBiomarkersHNF1BMaturity-onset diabetes of the youngMetabolomicsMODYPathogenesisPolycystic kidney disease

Identifiers

PMID35179657
PMCPMC8857088
OpenAlexW4212908396

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.