Evidence map›Paper›PMID 33934611›Full record

ReviewCirculation research2021

Preclinical Models of Cancer Therapy-Associated Cardiovascular Toxicity: A Scientific Statement From the American Heart Association.

Aarti Asnani, Javid J Moslehi, Bishow B Adhikari, Alan H Baik, Andreas M Beyer, Rudolf A de Boer, Alessandra Ghigo, Isabella M Grumbach, Salvia Jain, Han Zhu and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
8.2field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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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

11 authors.

Aarti Asnani
Javid J Moslehi
Bishow B Adhikari
Alan H Baik
Andreas M Beyer
Rudolf A de Boer
Alessandra Ghigo
Isabella M Grumbach
Salvia Jain
Han Zhu
American Heart Association Council on Basic Cardiovascular Sciences; Cardio-Oncology Science Subcommittee of Council on Genomic and Precision Medicine and Council on Clinical Cardiology; Council on Peripheral Vascular Disease; and Council on Arteriosclerosis, Thrombosis and Vascular Biology

Funding

Dissecting mechanisms of resistance underlying CD47-SIRPα inhibition in T-cell lymphomasK08CA230498 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, SALVIA · 2020 to 2024
$1.3M
CYP1 Inhibition as a New Therapeutic Strategy for Doxorubicin CardiomyopathyK08HL145019 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ASNANI, AARTI · 2019 to 2023
$837k
Sex-Specific Differences in the Development of Anthracycline CardiotoxicityR21HL148748 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ASNANI, AARTI · 2019 to 2020
$478k
NCI NIH HHS K08 CA230498NHLBI NIH HHS K08 HL145019NHLBI NIH HHS R21 HL148748
6 · The paper itself

Abstract

Although cardiovascular toxicity from traditional chemotherapies has been well recognized for decades, the recent explosion of effective novel targeted cancer therapies with cardiovascular sequelae has driven the emergence of cardio-oncology as a new clinical and research field. Cardiovascular toxicity associated with cancer therapy can manifest as a broad range of potentially life-threatening complications, including heart failure, arrhythmia, myocarditis, and vascular events. Beyond toxicology, the intersection of cancer and heart disease has blossomed to include discovery of genetic and environmental risk factors that predispose to both. There is a pressing need to understand the underlying molecular mechanisms of cardiovascular toxicity to improve outcomes in patients with cancer. Preclinical cardiovascular models, ranging from cellular assays to large animals, serve as the foundation for mechanistic studies, with the ultimate goal of identifying biologically sound biomarkers and cardioprotective therapies that allow the optimal use of cancer treatments while minimizing toxicities. Given that novel cancer therapies target specific pathways integral to normal cardiovascular homeostasis, a better mechanistic understanding of toxicity may provide insights into fundamental pathways that lead to cardiovascular disease when dysregulated. The goal of this scientific statement is to summarize the strengths and weaknesses of preclinical models of cancer therapy-associated cardiovascular toxicity, to highlight overlapping mechanisms driving cancer and cardiovascular disease, and to discuss opportunities to leverage cardio-oncology models to address important mechanistic questions relevant to all patients with cardiovascular disease, including those with and without cancer.

Indexed as

Toxicity TestsAmerican Heart AssociationAnimalsAntineoplastic AgentsCardiotoxicityCells, CulturedDisease Models, AnimalHeart DiseasesHumansMyocytes, CardiacRisk AssessmentUnited StatesAntineoplastic AgentsAHA Scientific Statementscardiotoxicityheart failuremedical oncologymodels, cardiovascularmyocarditisneoplasms

Identifiers

PMID33934611
PMCPMC8423100
OpenAlexW3159713747

What OpenQuestion holds

Textmetadata
LicenceTDM
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.