Evidence map›Paper›PMID 27717837›Full record

ReviewToxicology2016

An integrative view of cisplatin-induced renal and cardiac toxicities: Molecular mechanisms, current treatment challenges and potential protective measures.

George J Dugbartey, Luke J Peppone, Inge A M de Graaf

Open access · greenAbstract readReview
In one paragraph

Review in Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
14.3field-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

109 citing papers in PubMed, 217 citations in OpenAlex.

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49 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 3 institutions in 2 countries.

George J DugbarteyDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States; Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. Electronic address: profduu@yahoo.com.
Luke J PepponeDepartment of Surgery, University of Rochester Medical Center, School of Medicine and Dentistry, Rochester, NY, United States.
Inge A M de GraafDivision of Pharmacokinetics, Toxicology and Targeting, Department of Pharmacy, University of Groningen, Groningen, Netherlands.
University Medical Center Groningen · NLUniversity of Groningen · NLUniversity of Rochester Medical Center · US

Funding

URCC NCORP Research BaseUG1CA189961 · NCI · UNIVERSITY OF ROCHESTER · PI Michelle C Janelsins, KAREN M. MUSTIAN · 2014 to 2026
$67.7M
Management of Cancer-Treatment-Induced Bone LossK07CA168911 · NCI · UNIVERSITY OF ROCHESTER · PI PEPPONE, LUKE JOSEPH · 2013 to 2017
$724k
NCI NIH HHS K07 CA168911NCI NIH HHS UG1 CA189961
6 · The paper itself

Abstract

Cisplatin is currently one of the most widely-used chemotherapeutic agents against various malignancies. Its clinical application is limited, however, by inherent renal and cardiac toxicities and other side effects, of which the underlying mechanisms are only partly understood. Experimental studies show cisplatin generates reactive oxygen species, which impair the cell's antioxidant defense system, causing oxidative stress and potentiating injury, thereby culminating in kidney and heart failure. Understanding the molecular mechanisms of cisplatin-induced renal and cardiac toxicities may allow clinicians to prevent or treat this problem better and may also provide a model for investigating drug-induced organ toxicity in general. This review discusses some of the major molecular mechanisms of cisplatin-induced renal and cardiac toxicities including disruption of ionic homeostasis and energy status of the cell leading to cell injury and cell death. We highlight clinical manifestations of both toxicities as well as (novel)biomarkers such as kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). We also present some current treatment challenges and propose potential protective strategies including combination therapy with novel pharmacological compounds that might mitigate or prevent these toxicities, which include the use of hydrogen sulfide.

Indexed as

AnimalsAntineoplastic AgentsCardiotoxicityCisplatinDNA DamageHeart DiseasesHumansKidney DiseasesAntineoplastic AgentsCisplatinApoptosisCisplatinCisplatin-induced renal and cardiac toxicitiesInflammationReactive oxygen species

Identifiers

PMID27717837
PMCPMC5586594
OpenAlexW2529359491

What OpenQuestion holds

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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.