Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Biology Department, Morosky College of Health Professions and Sciences, Gannon University, Erie, PA, USA.
Mol Cell Endocrinol. 2019 May 1;487:66-74. doi: 10.1016/j.mce.2019.02.005. Epub 2019 Feb 14.
The peptide hormone relaxin is well-known for its anti-fibrotic actions in several organs, particularly from numerous studies conducted in animals. Acting through its cognate G protein-coupled receptor, relaxin family peptide receptor 1 (RXFP1), serelaxin (recombinant human relaxin) has been shown to consistently inhibit the excessive extracellular matrix production (fibrosis) that results from the aberrant wound-healing response to tissue injury and/or chronic inflammation, and at multiple levels. Furthermore, it can reduce established scarring by promoting the degradation of aberrant extracellular matrix components. Following on from the review that describes the mechanisms and signaling pathways associated with the extracellular matrix remodeling effects of serelaxin (Ng et al., 2019), this review focuses on newly identified tissue targets of serelaxin therapy in fibrosis, and the limitations associated with (se)relaxin research.
肽激素松弛素以其在几个器官中的抗纤维化作用而闻名，特别是在许多动物研究中。松弛素家族肽受体 1（RXFP1）是其同源 G 蛋白偶联受体，通过该受体，重组人松弛素（serelaxin）已被证明可一致抑制组织损伤和/或慢性炎症导致的异常伤口愈合反应所导致的细胞外基质过度产生（纤维化），并在多个水平上发挥作用。此外，它可以通过促进异常细胞外基质成分的降解来减少已形成的瘢痕。在描述与 serelaxin 的细胞外基质重塑作用相关的机制和信号通路的综述之后（Ng 等人，2019 年），本综述重点介绍了纤维化中 serelaxin 治疗的新鉴定的组织靶标，以及与（se）松弛素研究相关的局限性。
