Key result
Chemokines play a dual role in heart failure, acting as inflammatory mediators with a delicate balance between protective roles and damaging functions in the distressed myocardium.
This review highlights the complex, dual nature of chemokines in heart failure, balancing protective repair mechanisms with damaging inflammatory responses.
Dual chemokine roles in HF warrant therapeutic caution; leaves open selective pathway targeting for future trials.
The failing human heart is a bustling network of intra- and inter-cellular signals and related processes attempting to coordinate a repair mechanism for the injured or diseased myocardium. While our understanding of signaling by mode of cytokines is well understood on a systemic level, we are only now coming to elucidate the role of cytokines in cardiac self-regulation. An increasing number of studies are showing now that cardiomyocytes themselves have not only the ability but also the mandate to produce signals, and play direct roles in how these signals are interpreted. One of the families of cytokines employed by distressed cardiac tissue are chemokines. By regulating the movement of pro-inflammatory cell types to sites of injury, we see now how the myocardium responds to stress. Herein we review the participation of these inflammatory mediators and explore the delicate balance between their protective roles and damaging functions.
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Jarrah et al. (2015) conducted a review in Heart failure. Chemokines was evaluated. Chemokines play a dual role in heart failure, acting as inflammatory mediators with a delicate balance between protective roles and damaging functions in the distressed myocardium.
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