Evidence mapPaperPMID 40227235Full record

ReviewAntioxidants (Basel, Switzerland)2025

Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.

Antonio José Cabrera-Serrano, José Manuel Sánchez-Maldonado, Carmen González-Olmedo, María Carretero-Fernández, Leticia Díaz-Beltrán, Juan Francisco Gutiérrez-Bautista, Francisco José García-Verdejo, Fernando Gálvez-Montosa, José Antonio López-López, Paloma García-Martín and 4 more

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
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  7. [Mechanism of silibinin in renal injury induced by periodontitis in mice].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
    Article
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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

14 authors.

Antonio José Cabrera-SerranoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0003-0346-7960
José Manuel Sánchez-MaldonadoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
Carmen González-OlmedoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0001-8227-8900
María Carretero-FernándezGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0009-0003-8736-7146
Leticia Díaz-BeltránGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0002-6726-9456
Juan Francisco Gutiérrez-BautistaGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0003-1374-0756
Francisco José García-VerdejoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
Fernando Gálvez-MontosaGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
José Antonio López-LópezGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
Paloma García-MartínInstituto de Investigación Biosanitaria IBs.Granada, 18012 Granada, Spain.
Eva María PérezGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
Pedro Sánchez-RoviraGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.
Fernando Jesús Reyes-ZuritaGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0003-3438-0753
Juan SainzGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain.ORCID 0000-0002-9355-2423

Funding

Consejería de Transformación Económica, Industria, Conocimiento y Universidades and FEDER PY20/01282Instituto de Salud Carlos III - ISCIII (Spanish Government) co-funded by FEDER funds/European Regional Development Fund (ERDF) - a way to build Europe PI20/01845
6 · The paper itself

Abstract

Autophagy is a fundamental cellular process that maintains homeostasis by degrading damaged components and regulating stress responses. It plays a crucial role in cancer biology, including tumor progression, metastasis, and therapeutic resistance. Oxidative stress, similarly, is key to maintaining cellular balance by regulating oxidants and antioxidants, with its disruption leading to molecular damage. The interplay between autophagy and oxidative stress is particularly significant, as reactive oxygen species (ROS) act as both inducers and by-products of autophagy. While autophagy can function as a tumor suppressor in early cancer stages, it often shifts to a pro-tumorigenic role in advanced disease, aiding cancer cell survival under adverse conditions such as hypoxia and nutrient deprivation. This dual role is mediated by several signaling pathways, including PI3K/AKT/mTOR, AMPK, and HIF-1α, which coordinate the balance between autophagic activity and ROS production. In this review, we explore the mechanisms by which autophagy and oxidative stress interact across different hematological malignancies. We discuss how oxidative stress triggers autophagy, creating a feedback loop that promotes tumor survival, and how autophagic dysregulation leads to increased ROS accumulation, exacerbating tumorigenesis. We also examine the therapeutic implications of targeting the autophagy-oxidative stress axis in cancer. Current strategies involve modulating autophagy through specific inhibitors, enhancing ROS levels with pro-oxidant compounds, and combining these approaches with conventional therapies to overcome drug resistance. Understanding the complex relationship between autophagy and oxidative stress provides critical insights into novel therapeutic strategies aimed at improving cancer treatment outcomes.

Indexed as

autophagycancer treatment outcomescrosstalkhematological malignanciesoxidative stressreactive oxygen speciestherapeutic opportunities

Identifiers

PMID40227235
PMCPMC11939785

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.