Improvement of Sepsis by Hepatocyte Growth Factor, an Anti-Inflammatory Regulator: Emerging Insights and Therapeutic Potential

Table 1

Biological effects of HGF on target cells, involved in sepsis-related MOF.

Target cells	Effect	Involved mechanism	References
Epithelial cells
	Mitogenesis	Grab2-MAPK	[13]
	Migration	Gab1-PI3K	[13]
	Morphogen	Gab1-PI3K	[13]
	Anti-apoptosis	Bcl-xL induction	[15, 40]
Vascular cells
Endothelium	Mitogenesis	MAP-kinase	[10]
	Anti-inflammation	Anti-NF-κB	[32, 41–43]
	Anti-apoptosis	Bcl-2 upregulation	[10]
	Anti-coagulation	TM preservation	[44, 45]
Pericytes	Anti-proliferation	Anti-MAPK	[10, 15]
Immune cells
Macrophages	Anti-cytokine storm	HO-1 upregulation	[28, 29]
	Anti-NFκB activation	GSK3β de-phosphorylation	[46]
DC	Tolerogenic effects	TH1 ≪ TH2 balance	[10, 30]
Eosinophils	Anti-inflammation	Inhibition of eosinophilic toxin release	[10]
T-lymphocytes	Anti-proliferation	IFN-γ downregulation	[10]

Epithelial cells include hepatocytes, renal tubular cells, and alveolar and bronchial epithelium. TM: thrombomodulin; DC: dendritic cells; GSK3β: glycogen synthase kinase-3β. For abbreviations see text or original references.