Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26938939
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26938939
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Redox+Biol
2016 ; 8
(ä): 305-15
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Lung extracellular matrix and redox regulation
#MMPMID26938939
Watson WH
; Ritzenthaler JD
; Roman J
Redox Biol
2016[Aug]; 8
(ä): 305-15
PMID26938939
show ga
Pulmonary fibrosis affects millions worldwide and, even though there has been a
significant investment in understanding the processes involved in wound healing
and maladaptive repair, a complete understanding of the mechanisms responsible
for lung fibrogenesis eludes us, and interventions capable of reversing or
halting disease progression are not available. Pulmonary fibrosis is
characterized by the excessive expression and uncontrolled deposition of
extracellular matrix (ECM) proteins resulting in erosion of the tissue structure.
Initially considered an 'end-stage' process elicited after injury, these events
are now considered pathogenic and are believed to contribute to the course of the
disease. By interacting with integrins capable of signal transduction and by
influencing tissue mechanics, ECM proteins modulate processes ranging from cell
adhesion and migration to differentiation and growth factor expression. In doing
so, ECM proteins help orchestrate complex developmental processes and maintain
tissue homeostasis. However, poorly controlled deposition of ECM proteins
promotes inflammation, fibroproliferation, and aberrant differentiation of cells,
and has been implicated in the pathogenesis of pulmonary fibrosis,
atherosclerosis and cancer. Considering their vital functions, ECM proteins are
the target of investigation, and oxidation-reduction (redox) reactions have
emerged as important regulators of the ECM. Oxidative stress invariably
accompanies lung disease and promotes ECM expression directly or through the
overproduction of pro-fibrotic growth factors, while affecting integrin binding
and activation. In vitro and in vivo investigations point to redox reactions as
targets for intervention in pulmonary fibrosis and related disorders, but studies
in humans have been disappointing probably due to the narrow impact of the
interventions tested, and our poor understanding of the factors that regulate
these complex reactions. This review is not meant to provide a comprehensive
review of this field, but rather to highlight what has been learned and to raise
interest in this area in need of much attention.
free
free
free
