Potential therapeutic effect of SO₂ on fibrosis
| Autor: | Xin-Bao, Wang, Hong, Cui, Jun-Bao, Du |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Inflammation
Myocardium Pulmonary Fibrosis Myocytes Smooth Muscle Apoptosis Fibroblasts Pulmonary Artery Vascular Remodeling Antioxidants Muscle Smooth Vascular Rats Vasodilation Oxidative Stress Cell Movement Hypertension Animals Humans Sulfur Dioxide Aspartate Aminotransferases Cell Proliferation Signal Transduction |
| Zdroj: | Histology and histopathology. 34(12) |
| ISSN: | 1699-5848 |
| Popis: | 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 SO₂ also mediates the process of fibrosis. Inhibition of endogenous SO₂ can aggravate small pulmonary artery remodeling and abnormal collagen accumulation. SO₂ treatment significantly improves pulmonary fibrosis and pulmonary arterial remodeling. Overexpression of the key enzymes associated with endogenous SO₂ generation, aspartate aminotransferase (AAT) 1 and AAT2, mimics the effect of SO₂ on the down-regulation of collagen synthesis, while AAT1 or AAT2 knockdown aggravates abnormal collagen accumulation in vascular smooth muscle cells (VSMCs). SO₂ 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 SO₂ are related to its antioxidant effect, anti-inflammation effect, improvement in cardiac function, and cell proliferation inhibition. Therefore, SO₂ has a potential therapeutic effect on fibrosis. |
| Databáze: | OpenAIRE |
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