@Article{ecn.2008.0127,
AUTHOR = {Marie-Caroline Le Bousse-Kerdilès, Marie-Claire Martyré, Michel Samson},
TITLE = {Cellular and molecular mechanisms underlying bone marrow and liver fibrosis: a review},
JOURNAL = {European Cytokine Network},
VOLUME = {19},
YEAR = {2008},
NUMBER = {2},
PAGES = {69--80},
URL = {http://www.techscience.com/ECN/v19n2/65935},
ISSN = {1952-4005},
ABSTRACT = {Chronic fibroproliferative diseases are an important cause of morbidity and mortality in the world.
Fibrotic diseases occur in a large variety of vital organs, and the process of fibrosis seems common to all tissues.
In all of fibrotic reactions, the underlying cellular and molecular mechanisms involve leukocyte infiltration, the
persistence of inflammation in the tissue, and the proliferation of cells with a myofibroblast phenotype. The
different cell types participating to this process sustain production of growth factors, proteolytic enzymes,
angiogenic factors, and fibrogenic cytokines, which together stimulate the deposition of connective tissue elements
that progressively destroy and remodel normal tissue architecture. This review focuses on the comparison of two,
major, chronic fibroproliferative diseases: the myelofibrosis which develops in bone marrow, a “fluid” tissue
producing circulating haematopoietic cells, and liver fibrosis, which demonstrates all the features of solid tissue
damage. We discuss the etiology and histological quantification of each type of fibrosis, the implication of cell
partners, cytokines and growth factors, animal models developed to study fibrosis, and antifibrotic therapies for
each of these two fibroproliferative disease models.},
DOI = {10.1684/ecn.2008.0127}
}