Evidence map›Paper›PMID 29743983›Full record

ReviewOxidative medicine and cellular longevity2018

Chemotherapeutic Drugs and Mitochondrial Dysfunction: Focus on Doxorubicin, Trastuzumab, and Sunitinib.

Stefania Gorini, Antonella De Angelis, Liberato Berrino, Natalia Malara, Giuseppe Rosano, Elisabetta Ferraro

Erratum issuedOpen access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
26.1field-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

162 citing papers in PubMed, 318 citations in OpenAlex.

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  9. Oxeiptosis - potential in cancer treatment?Expert reviews in molecular medicine · 2026
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102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Stefania GoriniLaboratory of Pathophysiology of Cachexia and Metabolism of Skeletal Muscle, IRCCS San Raffaele Pisana, 00166 Rome, Italy.ORCID 0000-0003-4182-9942
Antonella De AngelisDepartment of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.ORCID 0000-0001-8469-3403
Liberato BerrinoDepartment of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
Natalia MalaraBionem Laboratory, Department of Experimental and Clinical Medicine, Magna Graecia University, 88100 Catanzaro, Italy.
Giuseppe RosanoCardiovascular and Cell Sciences Institute, St George's, University of London, Cranmer Terrace, London, UK.
Elisabetta FerraroLaboratory of Pathophysiology of Cachexia and Metabolism of Skeletal Muscle, IRCCS San Raffaele Pisana, 00166 Rome, Italy.ORCID 0000-0002-9596-4624
IRCCS Ospedale San Raffaele · ITUniversity of Campania "Luigi Vanvitelli" · ITMagna Graecia University · ITSt George's, University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many cancer therapies produce toxic side effects whose molecular mechanisms await full elucidation. The most feared and studied side effect of chemotherapeutic drugs is cardiotoxicity. Also, skeletal muscle physiology impairment has been recorded after many chemotherapeutical treatments. However, only doxorubicin has been extensively studied for its side effects on skeletal muscle. Chemotherapeutic-induced adverse side effects are, in many cases, mediated by mitochondrial damage. In particular, trastuzumab and sunitinib toxicity is mainly associated with mitochondria impairment and is mostly reversible. Vice versa, doxorubicin-induced toxicity not only includes mitochondria damage but can also lead to a more robust and extensive cell injury which is often irreversible and lethal. Drugs interfering with mitochondrial functionality determine the depletion of ATP reservoirs and lead to subsequent reversible contractile dysfunction. Mitochondrial damage includes the impairment of the respiratory chain and the loss of mitochondrial membrane potential with subsequent disruption of cellular energetic. In a context of increased stress, AMPK has a key role in maintaining energy homeostasis, and inhibition of the AMPK pathway is one of the proposed mechanisms possibly mediating mitochondrial toxicity due to chemotherapeutics. Therapies targeting and protecting cell metabolism and energy management might be useful tools in protecting muscular tissues against the toxicity induced by chemotherapeutic drugs.

Indexed as

DoxorubicinHumansIndolesMitochondria, HeartPyrrolesSunitinibTrastuzumabDoxorubicinIndolesPyrrolesSunitinibTrastuzumab

Identifiers

PMID29743983
PMCPMC5878876
OpenAlexW2791893068

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.