ArticleCirculation2020
Cyclodextrin Prevents Abdominal Aortic Aneurysm via Activation of Vascular Smooth Muscle Cell Transcription Factor EB.
Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 96 citations in OpenAlex.
- Gut Dysbiosis, Sex, and Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysms.Current atherosclerosis reports · 2026Review
- Molecular MRI monitoring of cyclodextrin therapy in murine abdominal aortic aneurysms.Scientific reports · 2026Article
- An Extravascular Synergistic Cocktail Therapeutic Strategy Based on Lanifibranor Loaded Self-Healing Bioelastomer for Abdominal Aortic Aneurysms.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- TCF7L2 promotes abdominal aortic aneurysm through smooth muscle cell-mediated extracellular matrix remodeling.JCI insight · 2026Article
- Targeting pyroptosis to treat aortic aneurysms: From mechanism to drug discovery (Review).International journal of molecular medicine · 2026Review
- SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis.Nature communications · 2026Article
- NFS1 Regulates IDH2 to Attenuate Abdominal Aortic Aneurysms via Interacting With SP2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Comprehensive analysis for the role of macrophage-driven genes in abdominal aortic aneurysm.Cardiovascular diagnosis and therapy · 2026Article
- Cyclodextrins as Modulators of Regulated Cell Death: Implications for Immunometabolism and Therapeutic Innovation.Pharmaceutics · 2026Review
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- ZFP36 Protects against Abdominal Aortic Aneurysm Formation by Regulating Vascular Smooth Muscle Phenotypic Switch.Research (Washington, D.C.) · 2026Article
- CRISPR-MI and scRNA-Seq Reveal TREM2's Function in Monocyte Infiltration and Macrophage Apoptosis During Abdominal Aortic Aneurysm Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pharmacological Inhibition of Ferroptosis Attenuates Experimental Abdominal Aortic Aneurysm Formation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Brown remodeling of white adipose tissue protects against abdominal aortic aneurysm via batokine FSTL1.EMBO molecular medicine · 2025Article
- How transcription factors regulate apoptosis in endometriosis (Review).Molecular medicine reports · 2025Review
- Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development.Nature communications · 2025Article
- Hypertriglyceridemia as a Key Contributor to Abdominal Aortic Aneurysm Development and Rupture: Insights From Genetic and Experimental Models.Circulation · 2025Article
- Single-cell spatial transcriptomics unravels the cellular landscape of abdominal aortic aneurysm.JCI insight · 2025Article
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- Cytoplasmic and nuclear NFATc3 cooperatively contributes to vascular smooth muscle cell dysfunction and drives aortic aneurysm and dissection.Acta pharmaceutica Sinica. B · 2025Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAbdominal aortic aneurysm (AAA) is a severe aortic disease with a high mortality rate in the event of rupture. Pharmacological therapy is needed to inhibit AAA expansion and prevent aneurysm rupture. Transcription factor EB (TFEB), a master regulator of autophagy and lysosome biogenesis, is critical to maintain cell homeostasis. In this study, we aim to investigate the role of vascular smooth muscle cell (VSMC) TFEB in the development of AAA and establish TFEB as a novel target to treat AAA.
methodsThe expression of TFEB was measured in human and mouse aortic aneurysm samples. We used loss/gain-of-function approaches to understand the role of TFEB in VSMC survival and explored the underlying mechanisms through transcriptome and functional studies. Using VSMC-selective
resultsWe found that TFEB is downregulated in both human and mouse aortic aneurysm lesions. TFEB potently inhibits apoptosis in VSMCs, and transcriptome analysis revealed that TFEB regulates apoptotic signaling pathways, especially apoptosis inhibitor B-cell lymphoma 2. B-cell lymphoma 2 is significantly upregulated by TFEB and is required for TFEB to inhibit VSMC apoptosis. We consistently observed that TFEB deficiency increases VSMC apoptosis and promotes AAA formation in different mouse AAA models. Furthermore, we demonstrated that 2-hydroxypropyl-β-cyclodextrin, a clinical agent used to enhance the solubility of drugs, activates TFEB and inhibits AAA formation and progression in mice. Last, we found that 2-hydroxypropyl-β-cyclodextrin inhibits AAA in a VSMC TFEB-dependent manner in mouse models.
conclusionsOur study demonstrated that TFEB protects against VSMC apoptosis and AAA. TFEB activation by 2-hydroxypropyl-β-cyclodextrin may be a promising therapeutic strategy for the prevention and treatment of AAA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.