Relaxin and insulin-like peptide 3 (INSL3) — hormones known for roles in pregnancy and male reproduction — also regulate bone remodeling and muscle regeneration, potentially offering new approaches to osteoporosis and sarcopenia.
Dual musculoskeletal roles discoveredRelaxin promotes bone remodeling, ligament healing, and muscle regeneration — functions far beyond its known role as a pregnancy hormone
What the researchers found
Relaxin and insulin-like peptide 3 (INSL3) — two peptide hormones traditionally associated with pregnancy and testicular function — appear to play important roles in bone and muscle health. Relaxin is involved in bone remodeling (balancing bone formation and breakdown), helps heal injured ligaments, and promotes skeletal muscle regeneration. INSL3, a male-specific hormone from testicular Leydig cells, also participates in bone remodeling.
Both peptides may help explain sex differences in osteoporosis and sarcopenia risk, and could represent new therapeutic targets for musculoskeletal diseases.
Why it matters
Osteoporosis and sarcopenia (age-related muscle loss) affect hundreds of millions of people worldwide. Current treatments are limited. If relaxin and INSL3 genuinely influence bone and muscle health, they could open entirely new therapeutic avenues — particularly for age-related musculoskeletal decline and for understanding why men and women experience these conditions differently.
The numbers in context
Review article — no primary experimental data presented
How the study worked
This is a narrative review synthesizing published preclinical and clinical evidence on relaxin and INSL3 in the musculoskeletal system. The authors examined cell culture studies, animal models, and available clinical data to build a case for these peptides' roles in bone remodeling, ligament healing, and muscle regeneration.
Who was studied
Review of preclinical and clinical literature (no primary study population)
What this study cannot tell us
As a narrative review, this does not present new experimental data. Much of the evidence comes from animal models and cell studies — clinical evidence in humans is still limited. The review is part of a themed journal section on relaxin family peptides, which may introduce selection bias toward positive findings. No systematic search methodology is described.
How to read the evidence
This is a narrative review that synthesizes mostly preclinical evidence (animal and cell studies). While published in a high-quality pharmacology journal, it presents no new data and the clinical evidence for musculoskeletal applications remains limited.
When this study was published
Published in 2017. The relaxin field has continued to advance since this review. Some of the therapeutic hypotheses discussed may have been further tested in the intervening years. The foundational biology described remains relevant.
The bigger picture
The musculoskeletal system is regulated by a complex network of hormones, and we're still discovering new players. Relaxin has already attracted attention for cardiovascular and fibrosis applications — if its bone and muscle effects are confirmed clinically, it could become a multi-indication peptide therapeutic. INSL3's role adds to our understanding of why men and women age differently in terms of bone and muscle mass.
Questions still open
- Could relaxin-based therapies prevent or reverse age-related bone loss and muscle wasting in humans?
- Does declining INSL3 in aging men contribute to their increasing osteoporosis and sarcopenia risk?
- How do relaxin and INSL3 interact with established musculoskeletal regulators like estrogen and testosterone?
Common questions
What is relaxin and what does it normally do?
Could relaxin or INSL3 be used to treat osteoporosis?
Read the original research
Relaxin and insulin-like peptide 3 in the musculoskeletal system: from bench to bedside.
British journal of pharmacology, 174(10), 1015-1024
Citation
Ferlin, Alberto; De Toni, Luca; Sandri, Marco; Foresta, Carlo. (2017). Relaxin and insulin-like peptide 3 in the musculoskeletal system: from bench to bedside.. British journal of pharmacology, 174(10), 1015-1024. https://doi.org/10.1111/bph.13490