Rln1, or relaxin-1, is a peptide-hormone-encoding gene belonging to the relaxin/insulin-like (RLN/INSL) gene family. It has diverse functions, such as regulating normal collagen turnover [5]. Rln1 is involved in multiple biological processes related to reproduction, like nipple development, parturition, and it may also play a role in the central nervous system [3,5]. Genetic models, especially gene-knockout (KO) mice, have been crucial for studying its functions.

Rln1-deficient mice exhibit abnormal nipple development, prolonged parturition, age-related pulmonary fibrosis, and abnormalities in the testis and prostate [3,4]. In female Rln1 -/- mice, there are issues with nipple development affecting their ability to feed progeny [3,4]. In the lungs, there is increased collagen accumulation and fibrosis [3,4]. In the context of heart failure with reduced ejection fraction (HFrEF), circulating RLN1 levels are significantly higher than in healthy controls, and RLN1 levels are inversely correlated with myocardial fibrosis [2]. In prostate cancer, a novel RLN1-RLN2 fusion transcript has been identified, and RLN1 expression is underrepresented in common PCa cell lines compared to normal and PCa tissue [1].

In conclusion, Rln1 plays essential roles in reproductive processes, collagen metabolism, and tissue fibrosis. The use of Rln1 KO mouse models has revealed its significance in diseases such as pulmonary fibrosis, HFrEF, and prostate cancer. These findings contribute to understanding the biological functions of Rln1 and may provide insights for potential therapeutic strategies targeting these disease areas.