MINI REVIEW article
Front. Immunol.
Sec. Molecular Innate Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1654622
This article is part of the Research TopicDevelopment of Diagnostic and Therapeutic Biomarkers for Tumors and Inflammation Based on Multi-omics Approaches Including Transcriptomics, Proteomics, and MetabolomicsView all 4 articles
The Innate Immune Axis Drives Aortic Dissection Pathogenesis Through Inflammation and Presents Novel Therapeutic Targets
Provisionally accepted
- 1Department of Cardiac Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China, Nanjing, China
- 2Institute of Cardiothoracic Vascular Disease, Nanjing University, Nanjing, China, Nanjing, China
- 3Department of Radiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China, Nanjing, China
- 4Nanjing University Medical School, Nanjing,210008, China, Nanjing, China
- 5Department of Cardiology, German Heart Centre Munich, Technical University of Munich, Munich 80636, Germany, Munich, Germany
- 6Deutsches Zentrum für Herz- und Kreislaufforschung (DZHK), Partner Site Munich Heart Alliance, Munich, Germany, Munich, Germany
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Acute aortic dissection (AAD) is a life-threatening cardiovascular emergency characterized by aortic layer separation and false lumen formation, with high mortality rates. Emerging evidence highlights the critical role of innate immunity in AD pathogenesis. Innate immune activation drives AAD progression through multiple mechanisms, including macrophage polarization (M1/M2 imbalance), neutrophil extracellular trap (NET) formation, and inflammasome activation. These processes amplify vascular inflammation via cytokine storms (IL-1β, IL-6, TNF-α) and oxidative stress, further promoting matrix metalloproteinase activation and smooth muscle cell phenotypic switching. The cGAS-STING pathway, triggered by mitochondrial DNA release, and TLR signaling act as central hubs connecting vascular injury to innate immune responses. This review synthesizes recent advances in the molecular mechanisms of AAD, focusing on aortic wall structural alterations, dysregulated signaling pathway, including TGF-β, Ang II, STING, and TLR cascades, and immune-inflammatory responses mediated by innate immune components. A deeper understanding of these innate immune components may lead to improved diagnostic biomarkers and targeted therapies for AAD management.
Keywords: Acute Aortic Dissection, Macrophage polarization, Neutrophil, Inflammation, Extracellularmatrix, Cytokines
Received: 26 Jun 2025; Accepted: 01 Sep 2025.
Copyright: © 2025 Xu, Chen, Nie, Xu, Feng, Chen and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dongjin Wang, Department of Cardiac Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China, Nanjing, China
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