Evidence mapPaperPMID 39200188Full record

ArticleBiomedicines2024

Unraveling the Complex Molecular Interplay and Vascular Adaptive Changes in Hypertension-Induced Kidney Disease.

Lyubomir Gaydarski, Iva N Dimitrova, Stancho Stanchev, Alexandar Iliev, Georgi Kotov, Vidin Kirkov, Nikola Stamenov, Tihomir Dikov, Georgi P Georgiev, Boycho Landzhov

Abstract read
In one paragraph

Article in Biomedicines, 2024. 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. Article
  3. Review
  4. Review
  5. The Apelinergic System in Kidney Disease: Novel Perspectives.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  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

10 authors.

Lyubomir GaydarskiDepartment of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.ORCID 0000-0003-4774-6507
Iva N DimitrovaDepartment of Cardiology, University Hospital "St. Ekaterina", Medical University of Sofia, 1431 Sofia, Bulgaria.
Stancho StanchevDepartment of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.
Alexandar IlievDepartment of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.
Georgi KotovDepartment of Rheumatology, Clinic of Rheumatology, University Hospital "St. Ivan Rilski", Medical Faculty, Medical University of Sofia, 1612 Sofia, Bulgaria.ORCID 0000-0001-7592-2497
Vidin KirkovDepartment of Health Policy and Management, Faculty of Public Health "Prof. Dr. Tzekomir Vodenicharov", Medical University of Sofia, 1431 Sofia, Bulgaria.
Nikola StamenovDepartment of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.
Tihomir DikovDepartment of General and Clinical Pathology, Medical University of Sofia, 1431 Sofia, Bulgaria.
Georgi P GeorgievDepartment of Orthopedics and Traumatology, University Hospital Queen Giovanna-ISUL, Medical University of Sofia, 1527 Sofia, Bulgaria.ORCID 0000-0001-8343-0337
Boycho LandzhovDepartment of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD.

Indexed as

angiogenesisapelin receptorarterial hypertensionneuronal nitric oxide synthasevascular adaptive mechanismsvascular endothelial growth factor

Identifiers

PMID39200188
PMCPMC11351430

What Socratic holds

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Registered trials

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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 Socratic graph.