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July 4, 2018Journal of Cellular and Molecular MedicineOpen Access

Signalling through Src family kinase isoforms is not redundant in models of thrombo‐inflammatory vascular disease

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Why the study?

Does the loss of individual SFK isoforms (Fgr or Lyn) reduce atherosclerotic disease burden in ApoE-/- mice?

Population

Single SFK knockout mice crossed with the ApoE-/- model of atherosclerosis, and in vitro adhesion assays

Comparison

Genetic deletion of single SFK isoforms vs ApoE-/- mice with intact SFK (implied)

Design

Preclinical

Authors

MHMatthew HarrisonVictorian Curriculum and Assessment AuthorityMCMyriam ChimenNestlé (Switzerland)MHMohammed T. HussainQueen Mary University of London

Discussion

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Implication

No change to clinical practice; leaves open whether isoform-specific SFK inhibition reduces human atherosclerotic burden.

Structured PICO

Does the loss of individual SFK isoforms (Fgr or Lyn) reduce atherosclerotic disease burden in ApoE-/- mice?

P
Population
Single SFK knockout mice crossed with the ApoE-/- model of atherosclerosis, and in vitro adhesion assays
I
Intervention
Genetic deletion of single SFK isoforms (Fgr or Lyn)
C
Comparator
ApoE-/- mice with intact SFK (implied)
O
Outcome
Platelet-dependent recruitment of monocytes and burden of atherosclerotic diseasesurrogate

Individual Src family kinases (Fgr and Lyn) operate in a non-redundant manner to regulate platelet-dependent monocyte recruitment and atherosclerotic disease burden, highlighting them as potential therapeutic targets.

Cite This Study

Harrison et al. (2018) studied this question.

synapsesocial.com/papers/6a7e2d2e18c0a3d0f08f4397https://doi.org/10.1111/jcmm.13721

Topics

Coronary artery disease
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