Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis

Table 1 Summary of Inflammatory and fibrotic cytokines and growth factors (detected in pericardial fluid) likely to modulate the pathophysiological processes leading to chronic fibrosis in the pericardium

Inflammatory/ fibrotic mediator	Major roles in Inflammation and fibrosis	References
TGF-β	Anti-inflammatory mediator	[17,37,46,61]
	ECM deposition and remodelling
CTGF	Myofibroblast activation	[17]
	ECM deposition and remodelling
TNF-α	Inducer and regulator of inflammation	[37,38]
	Macrophage and Natual Killer cell recruitment
IL-6	Late role in inflammatory cascade	[37,38]
	Adaptive Immune system activation
IL-8	Later role in inflammatory cascade Neutrophil cell recruitment	[37,38]
IL-10	Inflammatory mediator	[46]
IFN-γ	Immune response modulation Macrophage and Natual Killer cell activation Anti-fibrotic	[37-39,46,62]
VEGF	Angiogenesis and fibrosis promotion Fibrosis resolution	[39]
bFGF	ECM deposition	[23,39]
Ac-SDKP	Major role in the inhibition of fibrosis	[49]
Galectin-3	Myofibroblast activation ECM deposition	[49]

TGF-β: Growth factor β; CTGF: Connective tissue growth factor; TNF-α: Tumor necrosis factor-α; IFN-γ: Interferon-γ; VEGF: Vascular endothelial growth factor; bFGF: Basic fibroblast growth factor; ECM: Extracellular matrix.