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Cardiovascular Research Advance Access first published online on October 4, 2009
This version [Corrected Proof] published online on October 28, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp327
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Monocytes in heart failure: relationship to a deteriorating immune overreaction or a desperate attempt for tissue repair?

Stavros Apostolakis, Gregory Y.H. Lip and Eduard Shantsila*

Haemostasis Thrombosis and Vascular Biology Unit, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham B18 7QH, UK

* Corresponding author. Tel: +44 121 5075080, Fax: +44 121 5544083, Email: eduard.shantsila{at}swbh.nhs.uk

Monocytes play an important role in immune defence, inflammation, and tissue remodelling. Nevertheless, the role of monocytes in cardiovascular disease is obscure. Indeed, monocytes infiltrate dysfunctional tissue and augment tissue damage and are actively involved in tissue regeneration and healing. In support of the latter, recent studies have provided data on the functional and structural plasticity of monocytes. Monocytes are also actively involved in processes associated with tissue regeneration such as angiogenesis and vasculogenesis, either by producing pro-angiogenic factors or even by evolving to structural components of the vascular wall. This review article provides an overview on whether monocytes represent deteriorating immune overreaction in heart failure (HF), or a desperate attempt for tissue repair or physiological compensation in the failing heart. Perhaps, it is time to reconsider our attitude towards monocytes and consider more ‘monocyte activation’ rather than ‘monocyte suppression’ as a potential therapeutic target in HF.

KEYWORDS Monocytes; Heart failure; Angiogenesis; Inflammation; Endothelial progenitor cells

Time for primary review: 30 days


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