# Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction

**Authors:** Jieyan Wang, Hui Liang, Jie Fan

PMC · DOI: 10.1093/burnst/tkaf074 · 2025-11-20

## TL;DR

This paper reviews how trauma causes inflammation and organ dysfunction, focusing on new insights into molecular patterns, cell death, and gut microbiota.

## Contribution

The paper highlights recent advances in understanding trauma-induced inflammation mechanisms and introduces new diagnostic and therapeutic approaches.

## Key findings

- Damage-associated molecular patterns play vital roles in trauma-induced inflammation.
- Trauma-induced cell death and gut microbiota influence organ dysfunction progression.
- Organ–organ cross-talk pathways are key in systemic inflammation after trauma.

## Abstract

Trauma represents a significant global health issue, often resulting in devastating and long-lasting effects on the body throughout a patient's life. Organ inflammation and dysfunction caused by trauma present additional challenges for clinicians. Therefore, understanding the cellular and molecular mechanisms of post-trauma systemic inflammation and organ dysfunction is essential for improving the management of trauma. This review aims to summarize current updates on the findings that explore different mechanisms of trauma-induced inflammation and organ dysfunction, highlighting the recent understanding of the vital roles of damage-associated molecular patterns, trauma-induced cell death, organ–organ cross-talk pathways, and the gut microbiota in the development and progression of post-traumatic systemic inflammation. We also discuss new approaches that can potentially guide further investigations of trauma diagnosis, treatment, and prognosis.

## Full-text entities

- **Diseases:** Trauma (MESH:D014947), inflammation (MESH:D007249), organ dysfunction (MESH:D009102)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12860207/full.md

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Source: https://tomesphere.com/paper/PMC12860207