Evidence map›Paper›PMID 38683121›Full record

ArticleAging2024

Iron retardation in lysosomes protects senescent cells from ferroptosis.

Yujing Feng, Huaiqing Wei, Meng Lyu, Zhiyuan Yu, Jia Chen, Xinxing Lyu, Fengfeng Zhuang

Erratum issuedAbstract read
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

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  19. Neuroferroptosis in health and diseases.Nature reviews. Neuroscience · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Yujing FengSchool of Laboratory Animal and Shandong Laboratory Animal Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Huaiqing WeiBiomedical Research College and Shandong Medicinal Biotechnology Centre, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Meng LyuSchool of Clinical and Basic Medical Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Zhiyuan YuSchool of Clinical and Basic Medical Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Jia ChenSchool of Radiology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong, China.
Xinxing LyuSchool of Clinical and Basic Medical Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Fengfeng ZhuangSchool of Laboratory Animal and Shandong Laboratory Animal Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, an iron-triggered modality of cellular death, has been reported to closely relate to human aging progression and aging-related diseases. However, the involvement of ferroptosis in the development and maintenance of senescent cells still remains elusive. Here, we established a doxorubicin-induced senescent HSkM cell model and found that both iron accumulation and lipid peroxidation increase in senescent cells. Moreover, such iron overload in senescent cells has changed the expression panel of the ferroptosis-response proteins. Interestingly, the iron accumulation and lipid peroxidation does not trigger ferroptosis-induced cell death. Oppositely, senescent cells manifest resistance to the ferroptosis inducers, compared to the proliferating cells. To further investigate the mechanism of ferroptosis-resistance for senescent cells, we traced the iron flux in cell and found iron arrested in lysosome. Moreover, disruption of lysosome functions by chloroquine and LLOMe dramatically triggered the senescent cell death. Besides, the ferroitinophagy-related proteins FTH1/FTL and NCOA4 knockdown also increases the senescent cell death. Thus, we speculated that iron retardation in lysosome of senescent cells is the key mechanism for ferroptosis resistance. And the lysosome is a promising target for senolytic drugs to selectively clear senescent cells and alleviate the aging related diseases.

Indexed as

Cellular SenescenceFerroptosisIronLysosomesCell LineChloroquineDoxorubicinFerritinsHumansIron OverloadLipid PeroxidationNuclear Receptor CoactivatorsOxidoreductasesChloroquineDoxorubicinFerritinsFTH1 protein, humanIronNCOA4 protein, humanNuclear Receptor CoactivatorsOxidoreductasesferritinophagyferroptosisiron accumulationlysosomesenescent cells

Identifiers

PMID38683121
PMCPMC11131988

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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.