Evidence map›Paper›PMID 33912577›Full record

ReviewFrontiers in medicine2021

Iron Metabolism: An Under Investigated Driver of Renal Pathology in Lupus Nephritis.

Ewa Wlazlo, Borna Mehrad, Laurence Morel, Yogesh Scindia

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Increased levels of systemic iron content in adult-onset interleukin-6 knockout mice.Redox report : communications in free radical research · 2026
    Article
  2. Review
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  5. Article
  6. Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Skin Aging and the Upcoming Role of Ferroptosis in Geroscience.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024
    Review
  15. Review
  16. Ferroptosis and secondary nephrosis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Review
  17. Review
  18. Review
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  20. 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

4 authors at 2 institutions in 1 country.

Ewa WlazloDepartment of Medicine, University of Virginia School of Medicine, Charlottesville, VA, United States.
Borna MehradDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, FL, United States.
Laurence MorelDepartment of Pathology, University of Florida, Gainesville, FL, United States.
Yogesh ScindiaDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, FL, United States.
University of Florida · USUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephritis is a common manifestation of systemic lupus erythematosus, a condition associated with inflammation and iron imbalance. Renal tubules are the work horse of the nephron. They contain a large number of mitochondria that require iron for oxidative phosphorylation, and a tight control of intracellular iron prevents excessive generation of reactive oxygen species. Iron supply to the kidney is dependent on systemic iron availability, which is regulated by the hepcidin-ferroportin axis. Most of the filtered plasma iron is reabsorbed in proximal tubules, a process that is controlled in part by iron regulatory proteins. This review summarizes tubulointerstitial injury in lupus nephritis and current understanding of how renal tubular cells regulate intracellular iron levels, highlighting the role of iron imbalance in the proximal tubules as a driver of tubulointerstitial injury in lupus nephritis. We propose a model based on the dynamic ability of iron to catalyze reactive oxygen species, which can lead to an accumulation of lipid hydroperoxides in proximal tubular epithelial cells. These iron-catalyzed oxidative species can also accentuate protein and autoantibody-induced inflammatory transcription factors leading to matrix, cytokine/chemokine production and immune cell infiltration. This could potentially explain the interplay between increased glomerular permeability and the ensuing tubular injury, tubulointerstitial inflammation and progression to renal failure in LN, and open new avenues of research to develop novel therapies targeting iron metabolism.

Indexed as

ferroptosisglomerulonephritisironlupus nephritisproximal renal tubular cellsSLE

Identifiers

PMID33912577
PMCPMC8071941
OpenAlexW3152513609

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.