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[Research progress of anti-fibrotic drugs that inhibit epithelial-mesenchymal transition in pulmonary fibrosis].
Zhang, L B; Zhao, N; Nong, Q Y.
Afiliação
  • Zhang LB; Department of Occupational Medical Laboratory of Guangdong Province Hospital For Occupational Disease Prevention And Treatment, Guangzhou 510300, China Acute Infectious Disease Control Department of Zengcheng Dstrict Center For Disease Control And Prevention, Guangzhou, 511399, China.
  • Zhao N; Department of Occupational Medical Laboratory of Guangdong Province Hospital For Occupational Disease Prevention And Treatment, Guangzhou 510300, China.
  • Nong QY; Department of Occupational Medical Laboratory of Guangdong Province Hospital For Occupational Disease Prevention And Treatment, Guangzhou 510300, China.
Article em Zh | MEDLINE | ID: mdl-36725301
ABSTRACT
Pulmonary fibrosis is the end-stage pathological change of lung diseases, which seriously affects the respiratory function of human body. A large number of studies at home and abroad have confirmed that epithelial-mesenchymal transition (EMT) is an important intermediate stage in the development of pulmonary fibrosis. Inhibition of multiple pathways upstream and downstream of EMT, such as the classical Smads pathway and non-Smads pathway of TGF-1 can effectively inhibit the process of EMT and alleviate pulmonary fibrosis. This article will review the main conclusions of the mechanism of action of EMT as a target to improve the pathology of pulmonary fibrosis so far, and provide a theoretical basis and research direction for further research and development of anti-pulmonary fibrosis drugs.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrose Pulmonar / Transição Epitelial-Mesenquimal / Antifibróticos Limite: Humans Idioma: Zh Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fibrose Pulmonar / Transição Epitelial-Mesenquimal / Antifibróticos Limite: Humans Idioma: Zh Ano de publicação: 2023 Tipo de documento: Article