Evidence map›Paper›PMID 31295873›Full record

ReviewInternational journal of molecular sciences2019

Mitochondrial Involvement in Cisplatin Resistance.

Veronica Cocetta, Eugenio Ragazzi, Monica Montopoli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
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  9. ACTG1 mediates cisplatin resistance in NSCLC through induction of mitochondrial fragmentation.Apoptosis : an international journal on programmed cell death · 2025
    Article
  10. Review
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  14. Review
  15. Upregulation of MMP3 Promotes Cisplatin Resistance in Ovarian Cancer.International journal of molecular sciences · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

27 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

3 authors at 1 institution in 1 country.

Veronica CocettaDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Largo Egidio Meneghetti 2, 35131 Padua, Italy.
Eugenio RagazziDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Largo Egidio Meneghetti 2, 35131 Padua, Italy.ORCID 0000-0002-0390-6823
Monica MontopoliDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Largo Egidio Meneghetti 2, 35131 Padua, Italy. monica.montopoli@unipd.it.ORCID 0000-0001-6182-4132
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is one of the worldwide anticancer drugs and, despite its toxicity and frequent recurrence of resistance phenomena, it still remains the only therapeutic option for several tumors. Circumventing cisplatin resistance remains, therefore, a major goal for clinical therapy and represents a challenge for scientific research. Recent studies have brought to light the fundamental role of mitochondria in onset, progression, and metastasis of cancer, as well as its importance in the resistance to chemotherapy. The aim of this review is to give an overview of the current knowledge about the implication of mitochondria in cisplatin resistance and on the recent development in this research field. Recent studies have highlighted the role of mitochondrial DNA alterations in onset of resistance phenomena, being related both to redox balance alterations and to signal crosstalk with the nucleus, allowing a rewiring of cell metabolism. Moreover, an important role of the mitochondrial dynamics in the adaptation mechanism of cancer cells to challenging environment has been revealed. Giving bioenergetic plasticity to tumor cells, mitochondria allow cells to evade death pathways in stressful conditions, including chemotherapy. So far, even if the central role of mitochondria is recognized, little is known about the specific mechanisms implicated in the resistance. Nevertheless, mitochondria appear to be promising pharmacological targets for overcoming cisplatin resistance, but further studies are necessary.

Indexed as

AnimalsAntineoplastic AgentsCell NucleusCisplatinDNA, MitochondrialDrug Resistance, NeoplasmHumansMitochondriaMitochondrial DynamicsMitophagyNeoplasmsSignal TransductionAntineoplastic AgentsCisplatinDNA, Mitochondrialcisplatinmitochondriamitochondrial dynamicsmtDNAresistance

Identifiers

PMID31295873
PMCPMC6678541
OpenAlexW2957166771

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.