Evidence map›Paper›PMID 37267686›Full record

ArticleRedox biology2023

Energy stress modulation of AMPK/FoxO3 signaling inhibits mitochondria-associated ferroptosis.

Sufang Zhong, Wenjin Chen, Bocheng Wang, Chao Gao, Xiamin Liu, Yonggui Song, Hui Qi, Hongbing Liu, Tao Wu, Rikang Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
31.3field-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

93 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. ASIV Attenuates Cisplatin-Induced Proximal Tubular Injury by Enhancing Mitochondrial Biogenesis and Mitophagy Through the ADRA1A/AMPK/FOXO3A Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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33 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

11 authors at 1 institution in 1 country.

Sufang ZhongDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Wenjin ChenDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Bocheng WangDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Chao GaoDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Xiamin LiuDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Yonggui SongKey Laboratory of Evaluation of Traditional Chinese Medicine Efficacy (Prevention and Treatment of Brain Disease with Mental Disorders); Key Laboratory of Depression Animal Model Based on TCM Syndrome, Jiangxi Administration of Traditional Chinese Medicine; Key Laboratory of TCM for Prevention and Treatment of Brain Diseases with Cognitive Dysfunction, Jiangxi University of Chinese Medicine, Nanchang, China.
Hui QiDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Hongbing LiuDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Tao WuDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China. Electronic address: wutao2002cn@163.com.
Rikang WangDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China. Electronic address: rkwang@pkuszh.com.
Baodong ChenDepartment of Neurosurgery, Peking University Shenzhen Hospital, Shenzhen, China; Jiangxi University of Traditional Chinese Medicine, Nanchang, China. Electronic address: bdchen@pkuszh.com.
Jiangxi University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells and ischemic diseases exhibit unique metabolic responses and adaptations to energy stress. Forkhead box O 3a (FoxO3a) is a transcription factor that plays an important role in cell metabolism, mitochondrial dysfunction and oxidative stress response. Although the AMP-activated protein kinase (AMPK)/FoxO3a signaling pathway plays a pivotal role in maintaining energy homeostasis under conditions of energy stress, the role of AMPK/FoxO3a signaling in mitochondria-associated ferroptosis has not yet been fully elucidated. We show that glucose starvation induced AMPK/FoxO3a activation and inhibited ferroptosis induced by erastin. Inhibition of AMPK or loss of FoxO3a in cancer cells under the glucose starvation condition can sensitize these cells to ferroptosis. Glucose deprivation inhibited mitochondria-related gene expression, reduced mitochondrial DNA(mtDNA) copy number, decreased expression of mitochondrial proteins and lowered the levels of respiratory complexes by inducing FoxO3a. Loss of FoxO3a promoted mitochondrial membrane potential hyperpolarization, oxygen consumption, lipid peroxide accumulation and abolished the protective effects of energy stress on ferroptosis in vitro. In addition, we identified a FDA-approved antipsychotic agent, the potent FoxO3a agonist trifluoperazine, which largely reduced ferroptosis-associated cerebral ischemia-reperfusion (CIR) injuries in rats through AMPK/FoxO3a/HIF-1α signaling and mitochondria-dependent mechanisms. We found that FoxO3a binds to the promoters of SLC7A11 and reduces CIR-mediated glutamate excitotoxicity through inhibiting the expression of SLC7A11. Collectively, these results suggest that energy stress modulation of AMPK/FoxO3a signaling regulates mitochondrial activity and alters the ferroptosis response. The regulation of FoxO3a by AMPK may play a crucial role in mitochondrial gene expression that controls energy balance and confers resistance to mitochondria-associated ferroptosis and CIR injuries.

Indexed as

AMP-Activated Protein KinasesFerroptosisAnimalsDNA, MitochondrialForkhead Box Protein O3GlucoseMitochondriaRatsSignal TransductionAMP-Activated Protein KinasesDNA, MitochondrialForkhead Box Protein O3GlucoseAMPKEnergy stressFerroptosisFoxO3aLipid peroxidation

Identifiers

PMID37267686
PMCPMC10244700
OpenAlexW4377862207

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.