Evidence map›Paper›PMID 39985023›Full record

ArticleCardiovascular diabetology2025

Deficiency in nucleoside diphosphate kinase B leads to endothelial activation of the hexosamine biosynthesis pathway and cardiac dysfunction.

Feng Shao, Johanna Wieland, Yixin Wang, Merve Keles, Zenghui Meng, Santosh Lomada, Miao Qin, Veronika Leiss, Abel Martin-Garrido, Manuela Fuhrmann and 5 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Nuclear Proteome Map of Mouse Heart Chambers.Molecular & cellular proteomics : MCP · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Feng Shao *Experimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Johanna Wieland *Experimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Yixin Wang *Experimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Merve KelesDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Zenghui MengDZHK (German Center of Cardiovascular Research), Partner Site Heidelberg/Mannheim, Mannheim, Germany.
Santosh LomadaExperimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Miao QinExperimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Veronika LeissDepartment of Pharmacology, Experimental Therapy and Toxicology, University of Tübingen, 72074 Tübingen, Germany.
Abel Martin-GarridoDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Manuela FuhrmannDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Yi QiuExperimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Felix A TrogischDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Christiane VettelExperimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany.
Joerg HeinekeDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Yuxi FengExperimental Pharmacology Mannheim, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Str. 13-17, 68167, Mannheim, Germany. Yuxi.feng@medma.uni-heidelberg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNucleoside diphosphate kinase B (NDPKB) deficiency in endothelial cells (ECs) promotes the activation of the hexosamine biosynthesis pathway (HBP), leading to vascular damage in the retina. The aim of this study was to investigate the consequences of NDPKB deficiency in the mouse heart.

methodsNDPKB deficient mice were used in the study. Echocardiography was employed to assess cardiac function in vivo. Characterization of contractility in hiPSC-derived cardiomyocytes (hiPSC-CMs) was measured with the IonOptix contractility system. Immunoblotting and immunofluorescence were carried out to analyze the expression and localization of proteins in cultured cells and left ventricles (LVs).

resultsNDPKB deficient mice displayed impaired glucose tolerance and increased heart weight compared to controls. Echocardiographic analysis revealed an increase in the diastolic diameter of the left ventricular posterior wall (LVPW), a decrease in the early diastolic mitral valve E and E' wave, and in the ratios of E/A and E'/A' in NDPKB deficient hearts, suggesting cardiac hypertrophy and diastolic dysfunction. In line with cardiac dysfunction, the phosphorylation of myocardial phospholamban (PLN) and the expression of sarcoplasmic/endoplasmic reticulum Ca

conclusionsDeficiency in NDPKB leads to endothelial activation of the HBP and cardiac dysfunction. Our findings may highlight the crucial role of proper endothelial HBP in maintaining cardiovascular homeostasis.

Indexed as

Endothelial CellsHexosaminesHypertrophy, Left VentricularMyocytes, CardiacNM23 Nucleoside Diphosphate KinasesVentricular Dysfunction, LeftVentricular Function, LeftAnimalsCalcium-Binding ProteinsCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionAtp2a2 protein, mouseCalcium-Binding ProteinsHexosaminesNM23 Nucleoside Diphosphate KinasesPhospholambanSarcoplasmic Reticulum Calcium-Transporting ATPasesCardiac dysfunctionCardiomyopathyDiabetic complicationsEndothelial cellsExtracellular matrixHexosamine biosynthesis pathwayhiPSC-CMNDPKBO-GlcNAcPre-diabetic

Identifiers

PMID39985023
PMCPMC11846329

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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.