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2016 ; 18
(1
): 269
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Profibrotic mediators in tendon disease: a systematic review
#MMPMID27863509
Morita W
; Snelling SJ
; Dakin SG
; Carr AJ
Arthritis Res Ther
2016[Nov]; 18
(1
): 269
PMID27863509
show ga
BACKGROUND: Tendon disease is characterized by the development of fibrosis.
Transforming growth factor beta (TGF-?), bone morphogenic proteins (BMPs) and
connective tissue growth factor (CTGF) are key mediators in the pathogenesis of
fibrotic disorders. The aim of this systematic review was to investigate the
evidence for the expression of TGF-?, BMPs and CTGF along tendon disease
progression and the response of tendon cells to these growth factors accordingly.
METHOD: We conducted a systematic screen of the scientific literature using the
Medline database. The search terms used were "tendon AND TGF-?," "tendon AND BMP"
or "tendon AND CTGF." Studies of human samples, animal tendon injury and overuse
models were included. RESULTS: Thirty-three studies were included. In eight
studies the expression of TGF-?, BMPs or CTGF was dysregulated in chronic
tendinopathy and tendon tear patient tissues in comparison with healthy control
tissues. The expression of TGF-?, BMPs and CTGF was increased and showed temporal
changes in expression in tendon tissues from animal injury or overuse models
compared with the healthy control (23 studies), but the pattern of upregulation
was inconsistent between growth factors and also the type of animal model. No
study investigated the differences in the effect of TGF-?, BMPs or CTGF treatment
between patient-derived cells from healthy and diseased tendon tissues. Tendon
cells derived from animal models of tendon injury showed increased expression of
extracellular matrix protein genes and increased cell signaling response to TGF-?
and BMP treatments compared with the control cells (two studies). CONCLUSION: The
expression of TGF-?, BMPs and CTGF in tendon tissues is altered temporally during
healing in animal models of tendon injury or overuse, but the transition during
the development of human tendon disease is currently unknown. Findings from this
systematic review suggest a potential and compelling role for TGF-?, BMPs and
CTGF in tendon disease; however, there is a paucity of studies analyzing their
expression and stimulated cellular response in well-phenotyped human samples.
Future work should investigate the dynamic expression of these fibrotic growth
factors and their interaction with tendon cells using patient samples at
different stages of human tendon disease.
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