期刊
CURRENT MOLECULAR MEDICINE
卷 22, 期 3, 页码 196-208出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1566524021666210309113650
关键词
Connective tissue; extracellular matrix (ECM); fibrosis; myofibroblasts; relaxin (RLX); RXFP1; sereleaxin; TGF-beta
资金
- Italian Space Agency [2018-14-U.0]
Relaxin, a potential medication for fibrotic diseases, has shown promising results in in vitro and in vivo studies by inhibiting fibrogenic pathways and activating fibrosis-generating cells. However, clinical trials have yielded inconclusive results. This review summarizes the molecular mechanisms of fibrosis and critically evaluates the clinical trials, identifying future opportunities for the therapeutic use of relaxin.
Relaxin (recombinant human relaxin-2 hormone; RLX-2; serelaxin) had raised expectations as a new medication for fibrotic diseases. A plethora of in vitro and in vivo studies have offered convincing demonstrations that relaxin promotes remodeling of connective tissue extracellular matrix mediated by inhibition of multiple fibrogenic pathways, especially the downstream signaling of transforming growth factor (TGF)-beta 1, a major pro-fibrotic cytokine, and the recruitment and activation of myofibroblasts, the main fibrosis-generating cells. However, all clinical trials with relaxin in patients with fibrotic diseases gave inconclusive results. In this review, we have summarized the molecular mechanisms of fibrosis, highlighting those which can be effectively targeted by relaxin. Then, we have performed a critical reappraisal of the clinical trials performed to date with relaxin as an anti-fibrotic drug, in order to highlight their key points of strength and weakness and to identify some future opportunities for the therapeutic use of relaxin, or its analogues, in fibrotic diseases and pathologic scarring which, in our opinion, deserve to be investigated.
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