Evidence map›Paper›PMID 30483817›Full record

ReviewCellular and molecular life sciences : CMLS2019

Targeting autophagy using metallic nanoparticles: a promising strategy for cancer treatment.

Marco Cordani, Álvaro Somoza

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
11.8field-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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Organelle-Targeting Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
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  19. Anticancer Mechanism ofPharmaceuticals (Basel, Switzerland) · 2024
    Review
  20. Review

30 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

2 authors at 1 institution in 1 country.

Marco CordaniInstituto Madrileño de Estudios Avanzados en Nanociencia (IMDEA Nanociencia), CNB-CSIC-IMDEA Nanociencia Associated Unit "Unidad de Nanobiotecnología", Madrid, Spain. marco.cordani@imdea.org.
Álvaro SomozaInstituto Madrileño de Estudios Avanzados en Nanociencia (IMDEA Nanociencia), CNB-CSIC-IMDEA Nanociencia Associated Unit "Unidad de Nanobiotecnología", Madrid, Spain. alvaro.somoza@imdea.org.ORCID http://orcid.org/0000-0001-9873-435X
Madrid Institute for Advanced Studies · ES

Funding

FACILITY FOR MED UNIV OF SC CTR FOR SUBST ABUSE RESEARCHC06DA007809 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BALLENGER, JAMES C · 1991 to 1991
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Consejería de Educación, Juventud y Deporte, Comunidad de Madrid IND2017/IND-7809Consejería de Educación, Juventud y Deporte, Comunidad de Madrid S2017/BMD-3867Fundación Científica Asociación Española Contra el Cáncer Singulares 2014Horizon 2020 Framework Programme 685795Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2017-87305-RMinisterio de Economía, Industria y Competitividad, Gobierno de España SEV-2016-0686
6 · The paper itself

Abstract

Despite the extensive genetic and phenotypic variations present in the different tumors, they frequently share common metabolic alterations, such as autophagy. Autophagy is a self-degradative process in response to stresses by which damaged macromolecules and organelles are targeted by autophagic vesicles to lysosomes and then eliminated. It is known that autophagy dysfunctions can promote tumorigenesis and cancer development, but, interestingly, its overstimulation by cytotoxic drugs may also induce cell death and chemosensitivity. For this reason, the possibility to modulate autophagy may represent a valid therapeutic approach to treat different types of cancers and a variety of clinical trials, using autophagy modulators, are currently employed. On the other hand, recent progress in nanotechnology offers plenty of tools to fight cancer with innovative and efficient therapeutic agents by overcoming obstacles usually encountered with traditional drugs. Interestingly, nanomaterials can modulate autophagy and have been exploited as therapeutic agents against cancer. In this article, we summarize the most recent advances in the application of metallic nanostructures as potent modulators of autophagy process through multiple mechanisms, stressing their therapeutic implications in cancer diseases. For this reason, we believe that autophagy modulation with nanoparticle-based strategies would acquire clinical relevance in the near future, as a complementary therapy for the treatment of cancers and other diseases.

Indexed as

AutophagyAMP-Activated Protein KinasesHumansMetal NanoparticlesNanomedicineNeoplasmsNeurodegenerative DiseasesTOR Serine-Threonine KinasesAMP-Activated Protein KinasesTOR Serine-Threonine KinasesAutophagyCancer therapyNanomaterialsNanomedicine

Identifiers

PMID30483817
PMCPMC6420884
OpenAlexW2903252747

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.