# Cartilage intermediate layer protein inhibits ligamentum flavum hypertrophy mediated by TGF-β1/SMAD3/SERPINE2 signaling pathway

## TL;DR

This study explores how a protein called CILP may help reduce ligament thickening in spinal disorders by targeting a specific signaling pathway.

## Contribution

The study identifies CILP as a novel regulator of ligamentum flavum hypertrophy via the TGF-β1/SMAD3/SERPINE2 pathway.

## Key findings

- CILP inhibits TGF-β1-induced fibrosis in ligamentum flavum hypertrophy.
- The TGF-β1/SMAD3/SERPINE2 pathway is a key mediator in ligamentum flavum hypertrophy.
- CILP's regulatory role was confirmed using bioinformatics, human samples, and experimental models.

## Abstract

Lumbar Spinal Stenosis (LSS), a degenerative disorder, greatly impacts the elderly, often leads to discomfort, neurological problems, and a diminished quality of life. Ligamentum flavum hypertrophy (LFH), a marked influencor in LSS, is characterized by fibrosis resulting from excessive extracellular matrix deposition, largely driven by the differentiation of fibroblasts and inflammatory processes. Transforming growth factor β1 (TGF-β1) is pivotal in the LFH advancement by promoting fibrosis, highlighting its potential as a target for therapeutic strategies. Cartilage intermediate layer protein (CILP), known to regulate TGF-β1 activity in other tissues, may have potential in mitigating LFH. This research explores the function of CILP in LFH through the use of sophisticated bioinformatics, human samples, and experimental models, identifying its regulatory influence via the TGF-β1/SMAD3/SERPINE2 pathway.

The online version contains supplementary material available at 10.1007/s00018-025-06051-7.