Your browser doesn't support javascript.
loading
Elucidating the Molecular Pathways and Therapeutic Interventions of Gaseous Mediators in the Context of Fibrosis.
Li, Aohan; Wu, Siyuan; Li, Qian; Wang, Qianqian; Chen, Yingqing.
Afiliação
  • Li A; Chronic Disease Research Center, Medical College, Dalian University, Dalian 116622, China.
  • Wu S; Chronic Disease Research Center, Medical College, Dalian University, Dalian 116622, China.
  • Li Q; Chronic Disease Research Center, Medical College, Dalian University, Dalian 116622, China.
  • Wang Q; Chronic Disease Research Center, Medical College, Dalian University, Dalian 116622, China.
  • Chen Y; Engineering Technology Research Center for The Utilization of Functional Components of Organic Natural Products, Dalian University, Dalian 116622, China.
Antioxidants (Basel) ; 13(5)2024 Apr 25.
Article em En | MEDLINE | ID: mdl-38790620
ABSTRACT
Fibrosis, a pathological alteration of the repair response, involves continuous organ damage, scar formation, and eventual functional failure in various chronic inflammatory disorders. Unfortunately, clinical practice offers limited treatment strategies, leading to high mortality rates in chronic diseases. As part of investigations into gaseous mediators, or gasotransmitters, including nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), numerous studies have confirmed their beneficial roles in attenuating fibrosis. Their therapeutic mechanisms, which involve inhibiting oxidative stress, inflammation, apoptosis, and proliferation, have been increasingly elucidated. Additionally, novel gasotransmitters like hydrogen (H2) and sulfur dioxide (SO2) have emerged as promising options for fibrosis treatment. In this review, we primarily demonstrate and summarize the protective and therapeutic effects of gaseous mediators in the process of fibrosis, with a focus on elucidating the underlying molecular mechanisms involved in combating fibrosis.
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article