Evidence map›Paper›PMID 36208406›Full record

ReviewJournal of nephrology2022

Hypoxia-inducible factor signaling in vascular calcification in chronic kidney disease patients.

Sidar Copur, Duygu Ucku, Mario Cozzolino, Mehmet Kanbay

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Role of hypoxia inducible factor HIF-1Global cardiology science & practice · 2023
    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

4 authors at 2 institutions in 2 countries.

Sidar CopurDepartment of Medicine, Koc University School of Medicine, 34010, Istanbul, Turkey.
Duygu UckuDepartment of Medicine, Koc University School of Medicine, 34010, Istanbul, Turkey.
Mario CozzolinoRenal Division, Department of Health Sciences, University of Milan, Milan, Italy.
Mehmet KanbayDivision of Nephrology, Department of Medicine, Koc University School of Medicine, Istanbul, Turkey. mkanbay@ku.edu.tr.ORCID 0000-0002-1297-0675
Koç University · TRUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) affects approximately 15% of the adult population in high-income countries and is associated with significant comorbidities, including increased vascular calcifications which is associated with a higher risk for cardiovascular events. Even though the underlying pathophysiology is unclear, hypoxia-inducible factor (HIF) signaling appears to play a central role in inflammation, angiogenesis, fibrosis, cellular proliferation, apoptosis and vascular calcifications which is influenced by multiple variables such as iron deficiency anemia, serum phosphorus and calcium levels, fibroblast growth factor-23 (FGF-23) and Klotho. Along with the growing understanding of the pathology, potential therapeutic alternatives have emerged including HIF stabilizers and SGLT-2 inhibitors. The aim of this review is to discuss the role of HIF signaling in the pathophysiology of vascular calcification in CKD patients and to identify potential therapeutic approaches.

Indexed as

Hypoxia-Inducible Factor 1Renal Insufficiency, ChronicVascular CalcificationAdultFibroblast Growth Factor-23Fibroblast Growth FactorsHumansSignal TransductionFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsHypoxia-Inducible Factor 1Cardiovascular eventsChronic kidney diseaseHypoxia-inducible factorVascular calcification

Identifiers

PMID36208406
OpenAlexW4303647721

What OpenQuestion holds

Textmetadata
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.