Pathogenesis of Aortic Aneurysm and Dissection

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Background

Aortic aneurysm and dissection (AAD) is a life-threatening condition due to a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the different layers of the aortic wall. Medial degeneration is a typical pathological feature of AAD. It is mainly characterized by "excessive loss" of smooth muscle cells (SMCs) and extracellular matrix remodeling. They promote the occurrence of middle layer degenerative diseases through complex interactions between cells and molecules. As it stands, apoptosis, inflammation and oxidative stress are considered as the main mechanism leading to the reduction of the number of SMCs. The "excessive loss" of SMCs is manifested by the reduction of the total number of SMCs and the number of contractive SMCs. It is believed that M1 type macrophages promote AAD formation mainly through the following mechanisms: inducing apoptosis of SMCs; Increase the secretion of inflammatory factors such as IL-6, IL-8 and IL-11 to recruit inflammatory cells (neutrophils, monocytes and macrophages) to further expand tissue inflammation. Neutrophil activation can promote local inflammation and increase the risk of aortic rupture by increasing the analysis of inflammatory factors such as IL-6. Therefore, inflammation is the mechanism of neutrophils promoting AAD. Oxidative stress is involved in AAD-related pathological processes such as endothelial dysfunction, smooth muscle cell proliferation, apoptosis, phenotypic transformation, and vascular remodeling. Genome and methylomics, transcriptomics, proteomics, metabolomics, and microbiologics are revealing the pathogenesis of AAD from the molecular level. The relationship between cell death and AAD has also gradually attracted academic attention.

This Research Topic is to introduce the latest achievements of the pathogenesis of AAD which may involve cell omics, autophagy, inflammation, extracellular matrix, degeneration, biomechanical failure and cell death. Research results such as innovative treatment methods in AAD that aim at surgical mode in TAAD, interventional way or new materials of interventional devices and novel treatment strategies are also welcome.

We welcome submissions on the following topics, but are not limited to:
- Pathogenesis of clinical phenotypes classified to Stanford type A aortic dissection (TAAD), Stanford type B aortic dissection (TBAD), post-dissection aortic aneurysm (PDAA) as well as aortic aneurysm
- AAD mechanisms related to omics, autophagy, inflammation, extracellular matrix, degeneration, biomechanical failure and cell death
- Innovative treatment strategies discussion for AAD accompanied by COVID-19, and rare events such as pregnancy-associated AAD, and complications of AAD, aortic rupture, stroke, renal failure, paraplegia, malperfusion, hypoperfusion and mental disorders

Keywords: aortic aneurysm and dissection (AAD), mechanism, pathogenesis, genetics, omics, phenomics, autophagy, cell death

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