Publication: Potential therapeutic effect of SO2 on fibrosis.
Authors
Wang, Xin Bao ; Cui, Hong ; Du, Jun Bao
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-169
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info:eu-repo/semantics/article
Description
Abstract
Fibrosis is a pathological feature of most
chronic diseases and leads to the dysfunction of various
organs. However, there is currently no effective method
for treating fibrosis. In recent years, a small gas, sulfur
dioxide (SO2), which can be generated endogenously in
mammals, has been found to have vasorelaxation
activity, improve cardiac function and decrease
myocardial injury. Endogenous SO 2 also mediates the
process of fibrosis. Inhibition of endogenous SO 2 can
aggravate small pulmonary artery remodeling and
abnormal collagen accumulation. SO 2 treatment
significantly improves pulmonary fibrosis and
pulmonary arterial remodeling. Overexpression of the
key enzymes associated with endogenous SO 2
generation, aspartate aminotransferase (AAT) 1 and
AAT2, mimics the effect of SO 2 on the down-regulation
of collagen synthesis, while AAT1 or AAT2 knockdown
aggravates abnormal collagen accumulation in vascular
smooth muscle cells (VSMCs). SO 2 also improves
myocardial fibrosis induced by myocardial infarction or
diabetes in rats, and inhibits myocardial fibroblast
proliferation and migration by the extracellular signal-
regulated protein kinase pathway. The mechanisms
underlying the inhibition of fibrosis by SO 2 are related
to its antioxidant effect, anti-inflammation effect,
improvement in cardiac function, and cell proliferation
inhibition. Therefore, SO 2 has a potential therapeutic
effect on fibrosis.
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