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Background <p>Inguinal hernia is a common disease and mesh repair has been established as the standard treatment. Matrix metalloproteinase-2 (MMP-2), leading to collagen degradation, is elevated in inguinal hernia patients. Interleukin-1β (IL-1β) has been reported to promote progressions of some diseases by upregulating MMP-2, but its potential role in development of inguinal hernia remains unclear.</p> Methods <p>The expression levels of IL-1β, MMP-2, and collagens were assessed in human clinical specimens. Human skin fibroblasts were used to perform in vitro experiments and functional assays to investigate the underlying molecular mechanisms.</p> Results <p>IL-1β expression was significantly upregulated in inguinal hernia tissues and demonstrated a positive correlation with MMP-2 levels. Functionally, IL-1β suppressed proliferation and migration of fibroblasts. Mechanistic investigations revealed that IL-1β activated p38 mitogen-activated protein kinase (MAPK) signaling pathway, leading to MMP-2 upregulation and subsequent extracellular matrix degradation, characterized by an altered collagen type I (COL I) / type III (COL III) ratio.</p> Conclusions <p>IL-1β induces abnormal collagen metabolism by upregulating MMP-2 expression through p38 MAPK pathway. This finding provides a novel mechanistic insight into the pathogenesis of inguinal hernia.</p>

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A mechanistic exploration of IL-1β / p38 MAPK / MMP-2 pathway in inguinal hernia: evidence from clinical specimens and in vitro model

  • 期刊论文

  • 发表日期：

    2026年3月31日

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  • Tengfei Shang,
  • Pengfei Bo,
  • Dan Du,
  • Yang Fu,
  • Dianchen Wang

摘要

Background

Inguinal hernia is a common disease and mesh repair has been established as the standard treatment. Matrix metalloproteinase-2 (MMP-2), leading to collagen degradation, is elevated in inguinal hernia patients. Interleukin-1β (IL-1β) has been reported to promote progressions of some diseases by upregulating MMP-2, but its potential role in development of inguinal hernia remains unclear.

Methods

The expression levels of IL-1β, MMP-2, and collagens were assessed in human clinical specimens. Human skin fibroblasts were used to perform in vitro experiments and functional assays to investigate the underlying molecular mechanisms.

Results

IL-1β expression was significantly upregulated in inguinal hernia tissues and demonstrated a positive correlation with MMP-2 levels. Functionally, IL-1β suppressed proliferation and migration of fibroblasts. Mechanistic investigations revealed that IL-1β activated p38 mitogen-activated protein kinase (MAPK) signaling pathway, leading to MMP-2 upregulation and subsequent extracellular matrix degradation, characterized by an altered collagen type I (COL I) / type III (COL III) ratio.

Conclusions

IL-1β induces abnormal collagen metabolism by upregulating MMP-2 expression through p38 MAPK pathway. This finding provides a novel mechanistic insight into the pathogenesis of inguinal hernia.