Evidence map›Paper›PMID 39422260›Full record

ArticleActa physiologica (Oxford, England)2025

Beyond hemoglobin: Critical role of 2,3-bisphosphoglycerate mutase in kidney function and injury.

Vera A Kulow, Kameliya Roegner, Robert Labes, Mumtaz Kasim, Susanne Mathia, Claudia S Czopek, Nikolaus Berndt, Philipp N Becker, Gohar Ter-Avetisyan, Friedrich C Luft and 8 more

Abstract read
In one paragraph

Article in Acta physiologica (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Whole Blood Transcriptomic Analysis of Sickle Cell Trait.European journal of haematology · 2026
    Article
  3. Article
  4. Identification and Screening of Lactate-Related Genes as Molecular Markers for Early Diagnosis of Steroid-Induced Osteonecrosis of the Femoral Head.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. BPGM shapes NFAT5-driven cellular responses.Cellular and molecular life sciences : CMLS · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

18 authors.

Vera A KulowCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.ORCID 0000-0002-4226-6697
Kameliya RoegnerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Robert LabesCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.ORCID 0000-0001-8179-1315
Mumtaz KasimCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Susanne MathiaCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Claudia S CzopekCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Nikolaus BerndtDepartment of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Philipp N BeckerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Gohar Ter-AvetisyanCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Friedrich C LuftExperimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID 0000-0002-8635-1199
Philipp EnghardCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Christian HinzeCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Jan KlockeCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Kai-Uwe EckardtCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Kai M Schmidt-OttCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.
Pontus B PerssonCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.
Christian RosenbergerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Medizinische Klinik m.S. Nephrologie und Internistische Intensivmedizin (CCM), Berlin, Germany.ORCID 0000-0003-4194-561X
Michael FählingCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Translationale Physiologie (CCM), Berlin, Germany.ORCID 0000-0003-1079-5049

Funding

Bundesministerium für Bildung und ForschungDeutsche Forschungsgemeinschaft
6 · The paper itself

Abstract

aim2,3-bisphosphoglycerate mutase (BPGM) is traditionally recognized for its role in modulating oxygen affinity to hemoglobin in erythrocytes. Recent transcriptomic analyses, however, have indicated a significant upregulation of BPGM in acutely injured murine and human kidneys, suggesting a potential renal function for this enzyme. Here we aim to explore the physiological role of BPGM in the kidney.

methodsA tubular-specific, doxycycline-inducible Bpgm-knockout mouse model was generated. Histological, immunofluorescence, and proteomic analyses were conducted to examine the localization of BPGM expression and the impact of its knockout on kidney structure and function. In vitro studies were performed to investigate the metabolic consequences of Bpgm knockdown under osmotic stress.

resultsBPGM expression was localized to the distal nephron and was absent in proximal tubules. Inducible knockout of Bpgm resulted in rapid kidney injury within 4 days, characterized by proximal tubular damage and tubulointerstitial fibrosis. Proteomic analyses revealed involvement of BPGM in key metabolic pathways, including glycolysis, oxidative stress response, and inflammation. In vitro, Bpgm knockdown led to enhanced glycolysis, decreased reactive oxygen species elimination capacity under osmotic stress, and increased apoptosis. Furthermore, interactions between nephron segments and immune cells in the kidney suggested a mechanism for propagating stress signals from distal to proximal tubules.

conclusionBPGM fulfills critical functions beyond the erythrocyte in maintaining glucose metabolism in the distal nephron. Its absence leads to metabolic imbalances, increased oxidative stress, inflammation, and ultimately kidney injury.

Indexed as

Bisphosphoglycerate MutaseMice, KnockoutAcute Kidney InjuryAnimalsHemoglobinsKidneyMaleMiceOxidative StressBisphosphoglycerate MutaseHemoglobins2,3‐bisphosphoglycerate mutase (BPGM)acute kidney injury (AKI)glycolysisinflammationoxidative stress responsereactive oxygen species (ROS)

Identifiers

PMID39422260
PMCPMC11674375

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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.