Evidence map›Paper›PMID 35325321›Full record

ReviewCellular and molecular life sciences : CMLS2022

Iron overload in alcoholic liver disease: underlying mechanisms, detrimental effects, and potential therapeutic targets.

Long-Xia Li, Fang-Fang Guo, Hong Liu, Tao Zeng

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
12.8field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Kupffer cells: Orchestrators of liver physiology.Liver research (Beijing, China) · 2026
    Review
  7. Article
  8. Article
  9. Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Frontiers in microbiology · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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.

Long-Xia LiInstitute of Toxicology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Fang-Fang GuoDepartment of Pharmacy, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Hong LiuInstitute of Toxicology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Tao ZengInstitute of Toxicology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China. zengtao@sdu.edu.cn.ORCID http://orcid.org/0000-0002-1145-2059
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China 81872653National Natural Science Foundation of China 82073585
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is a global public health challenge due to the high incidence and lack of effective therapeutics. Evidence from animal studies and ALD patients has demonstrated that iron overload is a hallmark of ALD. Ethanol exposure can promote iron absorption by downregulating the hepcidin expression, which is probably mediated by inducing oxidative stress and promoting erythropoietin (EPO) production. In addition, ethanol may enhance iron uptake in hepatocytes by upregulating the expression of transferrin receptor (TfR). Iron overload in the liver can aggravate ethanol-elicited liver damage by potentiating oxidative stress via Fenton reaction, promoting activation of Kupffer cells (KCs) and hepatic stellate cells (HSCs), and inducing a recently discovered programmed iron-dependent cell death, ferroptosis. This article reviews the current knowledge of iron metabolism, regulators of iron homeostasis, the mechanism of ethanol-induced iron overload, detrimental effects of iron overload in the liver, and potential therapeutic targets.

Indexed as

Iron OverloadLiver Diseases, AlcoholicAnimalsHepatocytesHumansIronIronAlcoholic liver diseaseFerroptosisHepcidinIron overload

Identifiers

PMID35325321
PMCPMC11071846
OpenAlexW4220871280

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.