Evidence map›Paper›PMID 25949934›Full record

ReviewWorld journal of nephrology2015

Oxidative stress as a potential causal factor for autoimmune hemolytic anemia and systemic lupus erythematosus.

Junichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Yoshihito Iuchi

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Carotenoids and Their Interaction with the Immune System.Antioxidants (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Murine models of autoimmune hemolytic anemia.Current opinion in hematology · 2018
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Junichi FujiiJunichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata-city, Yamagata 990-9585, Japan.
Toshihiro KurahashiJunichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata-city, Yamagata 990-9585, Japan.
Tasuku KonnoJunichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata-city, Yamagata 990-9585, Japan.
Takujiro HommaJunichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata-city, Yamagata 990-9585, Japan.
Yoshihito IuchiJunichi Fujii, Toshihiro Kurahashi, Tasuku Konno, Takujiro Homma, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata-city, Yamagata 990-9585, Japan.
Yamagata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidneys and the blood system mutually exert influence in maintaining homeostasis in the body. Because the kidneys control erythropoiesis by producing erythropoietin and by supporting hematopoiesis, anemia is associated with kidney diseases. Anemia is the most prevalent genetic disorder, and it is caused by a deficiency of glucose 6-phosphate dehydrogenase (G6PD), for which sulfhydryl oxidation due to an insufficient supply of NADPH is a likely direct cause. Elevated reactive oxygen species (ROS) result in the sulfhydryl oxidation and hence are another potential cause for anemia. ROS are elevated in red blood cells (RBCs) under superoxide dismutase (SOD1) deficiency in C57BL/6 mice. SOD1 deficient mice exhibit characteristics similar to autoimmune hemolytic anemia (AIHA) and systemic lupus erythematosus (SLE) at the gerontic stage. An examination of AIHA-prone New Zealand Black (NZB) mice, which have normal SOD1 and G6PD genes, indicated that ROS levels in RBCs are originally high and further elevated during aging. Transgenic overexpression of human SOD1 in erythroid cells effectively suppresses ROS elevation and ameliorates AIHA symptoms such as elevated anti-RBC antibodies and premature death in NZB mice. These results support the hypothesis that names oxidative stress as a risk factor for AIHA and other autoimmune diseases such as SLE. Herein we discuss the association between oxidative stress and SLE pathogenesis based mainly on the genetic and phenotypic characteristics of NZB and New Zealand white mice and provide insight into the mechanism of SLE pathogenesis.

Indexed as

Autoimmune hemolytic anemiaNew Zealand black miceNew Zealand white miceRed blood cellsSystemic lupus erythematosus

Identifiers

PMID25949934
PMCPMC4419130
OpenAlexW1967244099

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.