Evidence map›Paper›PMID 26506346›Full record

ReviewInternational journal of molecular sciences2015

The Role of Autophagy in Lupus Nephritis.

Linlin Wang, Helen Ka Wai Law

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. BioMed research international · 2020
    Article
  18. Review
  19. Article
  20. The Role of NETosis in Systemic Lupus Erythematosus.Journal of cellular immunology · 2019
    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

2 authors at 1 institution in 1 country.

Linlin WangDepartment of Health Technology and Informatics, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hunghom, Hong Kong, China. 13903160r@connect.polyu.hk.
Helen Ka Wai LawDepartment of Health Technology and Informatics, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hunghom, Hong Kong, China. hthelen@polyu.edu.hk.
Hong Kong Polytechnic University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease characterized by the generation of immune responses to self-antigens. Lupus nephritis is one of the most common and severe complications in SLE patients. Though the pathogenesis of lupus nephritis has been studied extensively, unresolved questions are still left and new therapeutic methods are needed for disease control. Autophagy is a conserved catabolic process through which cytoplasmic constituents can be degraded in lysosome and reused. Autophagy plays vital roles in maintaining cell homeostasis and is involved in the pathogenesis of many diseases. In particular, autophagy can affect almost all parts of the immune system and is involved in autoimmune diseases. Based on genetic analysis, cell biology, and mechanism studies of the classic and innovative therapeutic drugs, there are growing lines of evidence suggesting the relationship between autophagy and lupus nephritis. In the present review, we summarize the recent publications investigating the relationship between autophagy and lupus nephritis and provide a new perspective towards the pathogenesis of lupus nephritis.

Indexed as

Apolipoprotein L1ApolipoproteinsAutoantigensAutophagyHerpesvirus 4, HumanHumansKidneyLipoproteins, HDLLupus NephritisMacrophagesNeutrophilsPodocytesProtein Tyrosine Phosphatases, Non-ReceptorUltraviolet RaysAPOL1 protein, humanApolipoprotein L1ApolipoproteinsAutoantigensLipoproteins, HDLMTMR3 protein, humanProtein Tyrosine Phosphatases, Non-Receptorautophagylupus nephritissystemic lupus erythematosus

Identifiers

PMID26506346
PMCPMC4632796
OpenAlexW1748899284

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.