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Published on: October 17, 2017
The role of monocytes and inflammation in the pathophysiology of heart failure
Benjamin J Wrigley1, Gregory Y H Lip, Eduard Shantsila
1University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham B18 7QH, UK.
Insights
Inflammation and monocytes are key in heart failure (HF) pathophysiology. Understanding monocyte subsets and their role in HF can lead to new therapeutic strategies for this condition.
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- Inflammation plays a critical role in heart failure (HF).
- Elevated inflammatory cytokine levels in patients with left ventricular dysfunction indicate prognostic implications.
- Monocytes are central to the inflammatory cascade, producing cytokines and influencing tissue repair in HF.
Purpose of the Study:
- To review the role of monocytes and inflammation in heart failure.
- To focus on monocyte activation, mobilization, recruitment, and endothelial adherence in HF.
- To discuss the impact of monocytes on myocardial performance and potential therapeutic strategies.
Main Methods:
- Review of existing literature on inflammation and monocytes in heart failure.
- Analysis of monocyte heterogeneity and function in the context of HF.
- Examination of the mechanisms of monocyte activation, migration, and adherence.
Main Results:
- Monocyte activation in HF involves complex interactions with various molecular signals.
- Activated monocytes migrate to the myocardium, adhering to the endothelium before infiltration.
- Monocyte subsets exhibit distinct characteristics that may influence their specific roles in HF.
Conclusions:
- Monocyte heterogeneity is crucial for understanding their specific contributions to heart failure.
- Targeting inflammation and monocyte activation presents a promising therapeutic avenue for HF treatment.
- Further research into monocyte dynamics can inform novel treatment strategies for heart failure.
Abstract:
There is growing evidence to support an important role of inflammation in the underlying pathophysiology of heart failure (HF). Indeed, inflammatory cytokine levels are well recognized to be increased in patients with left ventricular dysfunction and appear to have prognostic implications. Monocytes play a pivotal role in the inflammatory cascade and are a major source of both pro- and anti-inflammatory cytokines. They are intimately involved in tissue damage and repair and an imbalance of these processes may have detrimental consequences for the failing myocardium. Importantly, monocytes comprise of distinct subsets with different cell surface markers and functional characteristics and this heterogeneity may be important in understanding their specific role in HF. In HF, monocyte activation involves interplay between pattern recognition molecules, endotoxins, cytokines, and acute phase proteins. Activated monocytes migrate to the myocardium in response to powerful chemokines, where they must then attach to the endothelial wall before infiltrating into the myocardium itself. This review article aims to discuss the role of monocytes and inflammation in HF, focusing on monocyte activation, mobilisation, recruitment and endothelial adherence, as well as the effects they may have on myocardial performance. The therapeutic modulation of inflammation and monocyte activation in HF treatment will also be reviewed.
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