ArticleJournal of advanced research2025
Sympathetic hyperinnervation drives abdominal aortic aneurysm development by promoting vascular smooth muscle cell phenotypic switching.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Neuro-Mechanical Regulation of Vascular Smooth Muscle Cell Behaviour Under Ageing-Associated Substrate Stiffness.Current issues in molecular biology · 2026Article
- Neuroimmune Dynamics in Diseases of the Arterial Wall: Mechanistic Foundations and Translational Prospects.Current atherosclerosis reports · 2026Review
- Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- The association between reduced hypothalamic subregion volume and aortic aneurysm risk: a Mendelian randomization and multi-omics study with clinical MRI validation.Frontiers in cardiovascular medicine · 2026Article
- Article
- Global Profiling of the Proteome and Acetylome in Mice with Abdominal Aortic Aneurysms.ACS omega · 2025Article
- Temporal effects of sympathetic denervation on aortic remodeling and rupture in experimental abdominal aortic aneurysm.American journal of physiology. Heart and circulatory physiology · 2025Article
- Mice Models for Peripheral Denervation to Enhance Vascular Regeneration.Tissue engineering. Part C, Methods · 2025Article
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Authors and funding
18 authors.
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Abstract
introductionSympathetic hyperinnervation plays an important role in modulating the vascular smooth muscle cell (VSMC) phenotype and vascular diseases, but its role in abdominal aortic aneurysm (AAA) is still unknown.
objectivesThis study aimed to investigate the role of sympathetic hyperinnervation in promoting AAA development and the underlying mechanism involved.
methodsWestern blotting and immunochemical staining were used to detect sympathetic hyperinnervation. We performed sympathetic denervation through coeliac ganglionectomy (CGX) and 6-OHDA administration to understand the role of sympathetic hyperinnervation in AAA and investigated the underlying mechanisms through transcriptome and functional studies. Sema4D knockout (Sema4D
resultsWe observed sympathetic hyperinnervation, the most important form of sympathetic neural remodeling, in both mouse AAA models and AAA patients. Elimination of sympathetic hyperinnervation by CGX or 6-OHDA significantly inhibited AAA development and progression. We further revealed that sympathetic hyperinnervation promoted VSMC phenotypic switching in AAA by releasing extracellular ATP (eATP) and activating eATP-P2rx4-p38 signaling. Moreover, single-cell RNA sequencing revealed that Sema4D secreted by osteoclast-like cells induces sympathetic nerve diffusion and hyperinnervation through binding to Plxnb1. We consistently observed that AAA progression was significantly ameliorated in Sema4D-deficient mice.
conclusionsSympathetic hyperinnervation driven by osteoclast-like cell-derived Sema4D promotes VSMC phenotypic switching and accelerates pathological aneurysm progression by activating the eATP/P2rx4/p38 pathway. Inhibition of sympathetic hyperinnervation emerges as a potential novel therapeutic strategy for preventing and treating AAA.
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