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2017 ; 13
(9
): 1109-1117
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Mesenchymal Stem Cell-Dependent Modulation of Liver Diseases
#MMPMID29104502
Gazdic M
; Arsenijevic A
; Markovic BS
; Volarevic A
; Dimova I
; Djonov V
; Arsenijevic N
; Stojkovic M
; Volarevic V
Int J Biol Sci
2017[]; 13
(9
): 1109-1117
PMID29104502
show ga
Acute liver failure and cirrhosis display sequential and overlapping severe
pathogenic processes that include inflammation, hepatocyte necrosis, and
fibrosis, carrying a high mortality rate. Mesenchymal stem cells (MSCs) are a
heterogeneous subset of stromal stem cells with immunonodulatory characteristics.
MSCs are considered to act through multiple mechanisms to coordinate a dynamic,
integrated response to liver inflammation and fibrosis, which prevents the
progressive distortion of hepatic architecture. Accordingly, MSCs as well as
their products have been investigated as a novel therapeutic approach for the
treatment of inflammatory and fibrotic liver diseases. In this review, we
highlight the current findings on the MSC-based modulation of liver inflammation
and fibrosis, and the possible use of MSCs in the therapy of immune-mediated
liver pathology. We briefly describe the cellular and molecular mechanisms
involved in MSC-dependent modulation of cytokine production, phenotype and
function of liver infiltrated inflammatory cells and compare effects of engrafted
MSCs versus MSC-generated conditioned medium (MSC-CM) in the therapy of acute
liver injury. In order to elucidate therapeutic potential of MSCs and their
products in modulation of chronic liver inflammation and fibrosis, we present the
current findings regarding pathogenic role of immune cells in liver fibrosis and
describe mechanisms involved in MSC-dependent modulation of chronic liver
inflammation with the brief overview of on-going and already published clinical
trials that used MSCs for the treatment of immune mediated chronic liver
diseases. The accumulating evidence shows that MSCs had a significant beneficial
effect in the treatment of immune-mediated liver diseases.