Impacts of molecular drivers in aortic dissection

Abstract

Background: Aortic dissection (AD) is a lethal cardiovascular emergency involving high mortality and disability. However, its specific pathogenesis remains to be elucidated.

Methods: A bibliometric analysis based on the Web of Science database, VOSviewer software and Citex platforms was conducted to have a knowledge of the development trends, frontiers and hot spots of AD. Subsequently, the top five AD-related genes from the titles and abstracts of published literature were searched. Lastly, the roles of the top five genes and their encoded proteins in the onset of AD were reviewed.

Results: The bibliometrics showed that most studies are exploring the molecular drivers related to AD, especially gene mutations. The top five AD-related genes were transforming growth factor-β (TGFB)-related genes, elastin (ELN), fibrillin-1 (FBN1), angiotensinogen (AGT) and matrix metalloproteinase 9 (MMP9). In particular, regulation of the structure of elastic fiber by TGFB-related genes, ELN and FBN1, appears to be the principal mechanism contributing to AD onset. Activation of the renin-angiotensin system is the principal mechanism by which AGT triggers AD. MMP9 promotes the formation and development of AD by degrading extracellular matrix components.

Conclusion: TGFB, ELN, FBN1, AGT and MMP9 are the five top molecular drivers of AD, providing a comprehensive mechanistic insight into AD.

Keywords

AGT / aortic dissection / ELN / FBN1 / MMP9 / molecular drivers / TGFB

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2024 The Author(s). Clinical and Translational Discovery published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.