ArticleSurgical endoscopy2026
A mechanistic exploration of IL-1β / p38 MAPK / MMP-2 pathway in inguinal hernia: evidence from clinical specimens and in vitro model.
Article in Surgical endoscopy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Toward precision hernia surgery: integrating biomarkers, genomics, quantitative imaging, and artificial intelligence in abdominal wall repair.Hernia : the journal of hernias and abdominal wall surgery · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInguinal 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.
methodsThe 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.
resultsIL-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.
conclusionsIL-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.