Assessment of adult rat cardiac fibroblast viability following chronic sunitinib treatment

Research output: Contribution to journalMeeting abstract

2 Citations (Scopus)

Abstract

The tyrosine kinase inhibitor sunitinib has dramatically improved cancer therapy in recent years however, this success has been marred by reports of associated cardiotoxicity. The effect of sunitinib on cardiac myocyte function has been extensively studied, yet little is known of wider ranging effects on cardiac non-myocytes. Cardiac fibroblasts (CF) are the most abundant cell type within the heart and are responsible for maintaining cardiac structure via extracellular matrix remodelling and for facilitating synchronised cardiac contraction. Here, we have investigated whether chronic sunitinib treatment adversely affects CF viability.
LanguageEnglish
PagesA6-A7
Number of pages2
JournalHeart
Volume105
Issue numbersuppl 4
DOIs
Publication statusPublished - 1 May 2019
Event14th British Society of Cardiovascular Magnetic Resonance Annual Meeting 2019 - Oxford, United Kingdom
Duration: 26 Mar 201927 Mar 2019

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Fibroblasts
Cardiac Myocytes
Protein-Tyrosine Kinases
Extracellular Matrix
sunitinib
Neoplasms
Therapeutics
Cardiotoxicity

Keywords

  • tyrosine kinase inhibitor
  • sunitinib
  • cardiac fibroblast

Cite this

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title = "Assessment of adult rat cardiac fibroblast viability following chronic sunitinib treatment",
abstract = "The tyrosine kinase inhibitor sunitinib has dramatically improved cancer therapy in recent years however, this success has been marred by reports of associated cardiotoxicity. The effect of sunitinib on cardiac myocyte function has been extensively studied, yet little is known of wider ranging effects on cardiac non-myocytes. Cardiac fibroblasts (CF) are the most abundant cell type within the heart and are responsible for maintaining cardiac structure via extracellular matrix remodelling and for facilitating synchronised cardiac contraction. Here, we have investigated whether chronic sunitinib treatment adversely affects CF viability.",
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Assessment of adult rat cardiac fibroblast viability following chronic sunitinib treatment. / McMullen, Calum J; Wood, Rachel A; Cunningham, Margaret R; Currie, Susan.

In: Heart , Vol. 105, No. suppl 4, 01.05.2019, p. A6-A7.

Research output: Contribution to journalMeeting abstract

TY - JOUR

T1 - Assessment of adult rat cardiac fibroblast viability following chronic sunitinib treatment

AU - McMullen, Calum J

AU - Wood, Rachel A

AU - Cunningham, Margaret R

AU - Currie, Susan

PY - 2019/5/1

Y1 - 2019/5/1

N2 - The tyrosine kinase inhibitor sunitinib has dramatically improved cancer therapy in recent years however, this success has been marred by reports of associated cardiotoxicity. The effect of sunitinib on cardiac myocyte function has been extensively studied, yet little is known of wider ranging effects on cardiac non-myocytes. Cardiac fibroblasts (CF) are the most abundant cell type within the heart and are responsible for maintaining cardiac structure via extracellular matrix remodelling and for facilitating synchronised cardiac contraction. Here, we have investigated whether chronic sunitinib treatment adversely affects CF viability.

AB - The tyrosine kinase inhibitor sunitinib has dramatically improved cancer therapy in recent years however, this success has been marred by reports of associated cardiotoxicity. The effect of sunitinib on cardiac myocyte function has been extensively studied, yet little is known of wider ranging effects on cardiac non-myocytes. Cardiac fibroblasts (CF) are the most abundant cell type within the heart and are responsible for maintaining cardiac structure via extracellular matrix remodelling and for facilitating synchronised cardiac contraction. Here, we have investigated whether chronic sunitinib treatment adversely affects CF viability.

KW - tyrosine kinase inhibitor

KW - sunitinib

KW - cardiac fibroblast

UR - https://heart.bmj.com/

U2 - 10.1136/heartjnl-2019-SCF.13

DO - 10.1136/heartjnl-2019-SCF.13

M3 - Meeting abstract

VL - 105

SP - A6-A7

JO - Heart

T2 - Heart

JF - Heart

SN - 1355-6037

IS - suppl 4

ER -