Evidence map›Paper›PMID 35916902›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2022

Uremic mouse model to study vascular calcification and "inflamm-aging".

Markus Tölle, Cornelia Henkel, Jaqueline Herrmann, Christoph Daniel, Milen Babic, Mengdi Xia, Anna M Schulz, Kerstin Amann, Markus van der Giet, Mirjam Schuchardt

Open access · hybridAbstract read
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.International journal of molecular sciences · 2024
    Article
  10. Review
  11. Review
  12. Review
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

10 authors at 3 institutions in 2 countries.

Markus Tölle *Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0001-9843-2132
Cornelia Henkel *Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.
Jaqueline HerrmannDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0003-1043-3945
Christoph DanielDepartment of Nephropathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Krankenhausstraße 8-10, 91054, Erlangen, Germany.ORCID 0000-0002-6803-4755
Milen BabicDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0001-6248-0570
Mengdi XiaDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0002-1211-3462
Anna M SchulzDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0002-0124-3472
Kerstin AmannDepartment of Nephropathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Krankenhausstraße 8-10, 91054, Erlangen, Germany.ORCID 0000-0001-6116-8315
Markus van der GietDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany. Markus.vanderGiet@charite.de.ORCID 0000-0003-3590-5451
Mirjam SchuchardtDepartment of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Cooperate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID 0000-0001-7388-9611
Humboldt-Universität zu Berlin · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DENorth Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcification and chronic inflammation of the vascular wall is a high-risk factor for cardiovascular mortality, especially in patients with chronic uremia. For the reduction or prevention of rapid disease progression, no specific treatment options are currently available. This study aimed to evaluate an adenine-based uremic mouse model for studying medial vessel calcification and senescence-associated secretory phenotype (SASP) changes of aortic tissue to unravel molecular pathogenesis and provide a model for therapy testing. The dietary adenine administration induced a stable and similar degree of chronic uremia in DBA2/N mice with an increase of uremia blood markers such as blood urea nitrogen, calcium, creatinine, alkaline phosphatase, and parathyroid hormone. Also, renal fibrosis and crystal deposits were detected upon adenine feeding. The uremic condition is related to a moderate to severe medial vessel calcification and subsequent elastin disorganization. In addition, expression of osteogenic markers as Bmp-2 and its transcription factor Sox-9 as well as p21 as senescence marker were increased in uremic mice compared to controls. Pro-inflammatory uremic proteins such as serum amyloid A, interleukin (Il)-1β, and Il-6 increased. This novel model of chronic uremia provides a simple method for investigation of signaling pathways in vascular inflammation and calcification and therefore offers an experimental basis for the development of potential therapeutic intervention studies.

Indexed as

Kidney Failure, ChronicUremiaVascular CalcificationAdenineAgingAnimalsDisease Models, AnimalInflammationMiceRatsRats, Sprague-DawleyAdenineCalcificationCardiovascularChronic inflammationChronic renal insufficiencyInflammationVascular calcification

Identifiers

PMID35916902
PMCPMC9402761
OpenAlexW4289443295

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.