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TGF-β/Smads通路转导蛋白在心力衰竭发病中的研究进展
  • 期刊名称:现代生物医学进展
  • 时间:0
  • 页码:462-467
  • 语言:中文
  • 分类:R541.61[医药卫生—心血管疾病;医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:[1]石河子大学医学院病生教研室/新疆地方与民族高发病教育部重点实验室,新疆石河子832002
  • 相关基金:基金项目:国家科学自然基金(30760077)
  • 相关项目:TGFβ1基因多态性与新疆哈萨克族和汉族原发性高血压的相关性研究
作者: 何芳|石晓鹏|
中文摘要:

转化生长因子-β(transforming growth factor-β,TGF-β)作用复杂,广泛参与哺乳动物的各种病理生理过程如影响细胞的增殖分化、参与心力衰竭发展。TGF-β信号通路关键的信号传导分子为胞浆蛋白Smads。TGF-β诱导分化心肌成纤维细胞,刺激胶原蛋白等细胞间质成分的合成,促进细胞间质的沉积和抑制弹性蛋白酶等的分泌,刺激蛋白酶抑制剂的表达,从而抑制Ⅰ型胶原成分的降解,促进心肌纤维化发展,进一步了解TGF-β/Smads通路转导蛋白的作用及机制,通过抑制TGF-β/Smads通路转导蛋白作为治疗新靶点为最终防止心力衰竭提供了新的思路。

英文摘要:

Transforming growth factor-βrole in the complex, the broad participation of various mammals pathophysiological processes including cell proliferation and differentiation, development of heart failure and so on.TGF-β signaling pathway signaling molecules critical for the cytoplasmic protein Smads. TGF-β-induced differentiation of cardiac fibroblasts to stimulate collagen and other cells in the synthesis of stromal components, and promote the deposition of interstitial cells and inhibit the secretion of elastase, such as to stimulate the expression ofprotease inhibitors, thereby inhibiting collagen type I degradation and promote the development of myocar- dial fibrosis, TGF-β/Smads access a better understanding of the role of protein transduction and mechanisms, by inhibiting TGF-β/Smads transduction protein as a new target for therapy, providing a new train of thought for the prevention of heart failure eventually.

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