Spatial transcriptomic analysis reveals spatial features in human Stanford type A aortic dissection

Stanford type A aortic dissection (AAD) is a life-threatening cardiovascular disease characterized by tearing in the aortic wall. Using spatial transcriptomics and multiplex immunofluorescence, we comprehensively analyzed ascending aortas from eight AAD patients across different severities and segments. We demonstrate that SPP1-driven inflammatory signaling intensifies with AAD severity, identifying a nine-gene, layer-anchored severity scale: MYL6/CALD1/MYH9 (mild); CCL2/CP/COL4A1 (moderate); and TMSB4X/ATP5F1E/PKM (severe). Importantly, the collagen-remodeling triad COL1A1/COL3A1/MMP2 is concurrently up-regulated in the brachiocephalic, left subclavian, and left common carotid arteries, often before the ascending aorta meets surgical diameter thresholds. These molecular signatures provide a critical foundation for non-invasive biomarker discovery, risk stratification, and precision pharmacotherapy targeting the SPP1-inflammatory axis, ultimately offering new insights into AAD mechanisms and therapeutic targets.

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Publication Details

Journal
iScience
Published
2026-07-16
DOI
https://doi.org/10.1016/j.isci.2026.116868
Primary Topic
Aortic Disease and Treatment Approaches
Type
article
Field-Weighted Citation Impact
0.00

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article

Spatial transcriptomic analysis reveals spatial features in human Stanford type A aortic dissection

Jun‐Yi Luo, Dilare Adi, Fen Liu, Ying Cao et al.
iScience
Aortic Disease and Treatment Approaches
article

Spatial transcriptomic analysis reveals spatial features in human Stanford type A aortic dissection

Jun‐Yi Luo, Dilare Adi, Fen Liu, Ying Cao, Qian Zhao, Yi‐Ning Yang, Xiao-Mei Li, Zheng Liu, Haizhou Liu, Yanhong Li, Di Liu, Li-Ying Wang, Qiang Huo
article en

Abstract

Stanford type A aortic dissection (AAD) is a life-threatening cardiovascular disease characterized by tearing in the aortic wall. Using spatial transcriptomics and multiplex immunofluorescence, we comprehensively analyzed ascending aortas from eight AAD patients across different severities and segments. We demonstrate that SPP1-driven inflammatory signaling intensifies with AAD severity, identifying a nine-gene, layer-anchored severity scale: MYL6/CALD1/MYH9 (mild); CCL2/CP/COL4A1 (moderate); and TMSB4X/ATP5F1E/PKM (severe). Importantly, the collagen-remodeling triad COL1A1/COL3A1/MMP2 is concurrently up-regulated in the brachiocephalic, left subclavian, and left common carotid arteries, often before the ascending aorta meets surgical diameter thresholds. These molecular signatures provide a critical foundation for non-invasive biomarker discovery, risk stratification, and precision pharmacotherapy targeting the SPP1-inflammatory axis, ultimately offering new insights into AAD mechanisms and therapeutic targets.

iScienceVol. 29(8)
Xinjiang Medical University (CN), Chinese Academy of Sciences (CN), First Affiliated Hospital of Xinjiang Medical University (CN), Wuhan Institute of Virology (CN), People's Hospital of Xinjiang Uygur Autonomous Region (CN), University of Chinese Academy of Sciences (CN), Xinjiang University (CN)
National Natural Science Foundation of China
Openalex Percentile: Top 9%
Aortic Disease and Treatment Approaches
DOIOpen Access PDFOpenAlex
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