Evidence map›Paper›PMID 41531728›Full record

ArticleiScience2026

HMOX1 drives dihydroartemisinin-sensitized ferroptosis antagonized by mitochondrial fusion.

Zi-Jie Deng, Jing Zhang, Zhang-Zhong Yang, Qing-Zhang Tuo, Peng Lei

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026
    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

5 authors.

Zi-Jie DengDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.
Jing ZhangDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.
Zhang-Zhong YangDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.
Qing-Zhang TuoDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.
Peng LeiDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Artemisinin is the key component of artemisinin-based combination therapy (ACT) for malaria. Combinations of artemisinin with partner drugs demonstrate significant therapeutic potential in various diseases, including cancer. However, the precise mechanisms by which artemisinin, in combination with partner drugs, induces cell death are still not fully understood. Ferroptosis, a distinct form of cell death characterized by its dependence on iron, oxygen, and phospholipids (PLs), represents one potential pathway. In this study, we discovered that dihydroartemisinin (DHA), the active metabolite of artemisinin and its derivatives, sensitizes cells to ferroptosis induced by GPX4 inhibition. Through integrated data analysis and experimental validation, we found that DHA enhances ferroptosis sensitivity by promoting heme oxygenase 1 (HMOX1, HO-1)-mediated mitochondrial oxidative stress, thereby triggering a feedback loop that promotes mitochondrial fusion. These results broaden our understanding of the mechanisms of DHA in combination with partner drugs, and provide insights for clinical translation of ferroptosis.

Indexed as

Drug delivery systemDrug dispensingPharmacologyTherapeutics

Identifiers

PMID41531728
PMCPMC12794436

What Socratic 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 Socratic graph.