Evidence map›Paper›PMID 30993878›Full record

ArticleJournal of cellular and molecular medicine2019

Augmenter of liver regeneration protects the kidney from ischaemia-reperfusion injury in ferroptosis.

Li-Li Huang, Xiao-Hui Liao, Hang Sun, Xiao Jiang, Qi Liu, Ling Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Ferroptosis: Disease Associations and Therapeutic Target Exploration.Journal of molecular neuroscience : MN · 2025
    Review
  6. Review
  7. Research progress of ferroptosis in acute kidney injury.Frontiers in cell and developmental biology · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Role of ferroptosis in chronic kidney disease.Cell communication and signaling : CCS · 2024
    Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Li-Li HuangDepartment of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Xiao-Hui LiaoDepartment of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Hang SunKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Department of Infectious Diseases, The Second Affiliated Hospital, Institute for Viral Hepatitis, Chongqing Medical University, Chongqing, People's Republic of China.
Xiao JiangDepartment of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Qi LiuKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Department of Infectious Diseases, The Second Affiliated Hospital, Institute for Viral Hepatitis, Chongqing Medical University, Chongqing, People's Republic of China.
Ling ZhangDepartment of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0002-8049-6231
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is a common and severe clinical condition with high morbidity and mortality. Ischaemia-reperfusion (I/R) injury remains the major cause of AKI in the clinic. Ferroptosis is a recently discovered form of programmed cell death (PCD) that is characterized by iron-dependent accumulation of reactive oxygen species (ROS). Compelling evidence has shown that renal tubular cell death involves ferroptosis, although the underlying mechanisms remain unclear. Augmenter of liver regeneration (ALR) is a widely distributed multifunctional protein that is expressed in many tissues. Our previous study demonstrated that ALR possesses an anti-oxidant function. However, the modulatory mechanism of ALR remains unclear and warrants further investigation. Here, to elucidate the role of ALR in ferroptosis, ALR expression was inhibited using short hairpin RNA lentivirals (shRNA) in vitro model of I/R-induced AKI. The results suggest that the level of ferroptosis is increased, particularly in the shRNA/ALR group, accompanied by increased ROS and mitochondrial damage. Furthermore, inhibition of system xc- with erastin aggravates ferroptosis, particularly silencing of the expression of ALR. Unexpectedly, we demonstrate a novel signalling pathway of ferroptosis. In summary, we show for the first time that silencing ALR aggravates ferroptosis in an in vitro model of I/R. Notably, we show that I/R induced kidney ferroptosis is mediated by ALR, which is linked to the glutathione-glutathione peroxidase (GSH-GPx) system.

Indexed as

Acute Kidney InjuryApoptosisCell LineFerroptosisHumansKidneyLiver RegenerationMitochondriaOxidative StressReactive Oxygen SpeciesReperfusion InjuryRNA, Small InterferingSignal TransductionReactive Oxygen SpeciesRNA, Small Interferingacute kidney injury (AKI)augmenter of liver regeneration (ALR)ferroptosisischaemia-reperfusion (I/R) injuryreactive oxygen species (ROS)

Identifiers

PMID30993878
PMCPMC6533476
OpenAlexW2939241471

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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 OpenQuestion graph.