期刊
JOURNAL OF BIOMEDICAL RESEARCH
卷 32, 期 1, 页码 3-12出版社
NANJING MEDICAL UNIV
DOI: 10.7555/JBR.31.20170034
关键词
systemic sclerosis; transforming growth factor-beta; mechanism; therapeutics
Systemic sclerosis (SSc) is a complex, multiorgan autoimmune disease of unknown etiology. Manifestation of the disease results from an interaction of three key pathologic features including irregularities of the antigen-specific immune system and the non-specific immune system, resulting in autoantibody production, vascular endothelial activation of small blood vessels, and tissue fibrosis as a result of fibroblast dysfunction. Given the heterogeneity of clinical presentation of the disease, a lack of universal models has impeded adequate testing of potential therapies for SSc. Regardless, recent research has elucidated the roles of various ubiquitous molecular mechanisms that contribute to the clinical manifestation of the disease. Transforming growth factor beta (TGF-beta) has been identified as a regulator of pathological fibrogenesis in SSc. Various processes, including cell growth, apoptosis, cell differentiation, and extracellular matrix synthesis are regulated by TGF-beta, a type of cytokine secreted by macrophages and many other cell types. Understanding the essential role TGF-beta pathways play in the pathology of systemic sclerosis could provide a potential outlet for treatment and a better understanding of this severe disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据