Evidence map›Paper›PMID 40070880›Full record

ReviewFrontiers in cell and developmental biology2025

Ferritinophagy: multifaceted roles and potential therapeutic strategies in liver diseases.

Kejia Wu, Wei Zhao, Zeyu Hou, Weigang Zhang, Lei Qin, Junyi Qiu, Daobin Wang, Lin Zhuang, Xiaofeng Xue, Ding Sun

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. 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

10 authors.

Kejia Wu *Department of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Wei Zhao *Department of Anesthesiology, Xinyi People's Hospital, Xinyi, Jiangsu, China.
Zeyu HouDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Weigang ZhangDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Lei QinDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Junyi QiuDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Daobin WangDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Lin ZhuangDepartment of General Surgery, Wujin Affiliated Hospital of Jiangsu University and The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu, China.
Xiaofeng XueDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Ding SunDepartment of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferritinophagy, the selective autophagic degradation of ferritin to release iron, is emerging as a critical regulator of iron homeostasis and a key player in the pathogenesis of various liver diseases. This review comprehensively examines the mechanisms, regulation, and multifaceted roles of ferritinophagy in liver health and disease. Ferritinophagy is intricately regulated by several factors, including Nuclear Receptor Coactivator 4 (NCOA4), Iron regulatory proteins and signaling pathways such as mTOR and AMPK. These regulatory mechanisms ensure proper iron utilization and prevent iron overload, which can induce oxidative stress and ferroptosis. In liver diseases, ferritinophagy exhibits dual roles. In liver fibrosis, promoting ferritinophagy in hepatic stellate cells (HSCs) can induce cell senescence and reduce fibrosis progression. However, in non-alcoholic fatty liver disease (NAFLD), chronic ferritinophagy may exacerbate liver injury through iron overload and oxidative stress. In hepatocellular carcinoma (HCC), ferritinophagy can be harnessed as a novel therapeutic strategy by inducing ferroptosis in cancer cells. Additionally, ferritinophagy is implicated in drug-induced liver injury and sepsis-associated liver damage, highlighting its broad impact on liver pathology. This review also explores the crosstalk between ferritinophagy and other selective autophagy pathways, such as mitophagy and lipophagy, which collectively influence cellular homeostasis and disease progression. Understanding these interactions is essential for developing comprehensive therapeutic strategies targeting multiple autophagy pathways. In summary, ferritinophagy is a complex and dynamic process with significant implications for liver diseases. This review provides an in-depth analysis of ferritinophagy's regulatory mechanisms and its potential as a therapeutic target, emphasizing the need for further research to elucidate its role in liver health and disease.

Indexed as

autophagyferritinophagyferroptosisHCCliver fibrosisNAFLD

Identifiers

PMID40070880
PMCPMC11893559

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.