ArticleCirculation2023
Bestrophin3 Deficiency in Vascular Smooth Muscle Cells Activates MEKK2/3-MAPK Signaling to Trigger Spontaneous Aortic Dissection.
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Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 37 citations in OpenAlex.
- Crosstalk between ubiquitination and other post-translational modifications in cardiovascular diseases.iScience · 2026Review
- BEST4⁺ cells: a potential hub of intestinal ion transport and diarrhea manipulation.Advanced biotechnology · 2026Review
- The Role of Cysteine-Rich Protein 2 in Aortic Dissection: Implications for VSMC Phenotypic Modulation-CSRP2 Impedes the Progression of Aortic Dissection.Biomolecules · 2026Article
- Vascular Sphingosine Kinase 1 Regulates Angiotensin II-Induced Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis.Nature communications · 2026Article
- Bioinformatics Analysis of Ferroptosis-Related Driver Genes in Stanford Type A Aortic Dissection.Current issues in molecular biology · 2026Article
- Sparcl1 mitigates abdominal aortic aneurysm through inhibiting lymphangiogenesis-mediated TLS formation.Nature immunology · 2026Article
- MEKK3 bridges gut-brain communication and cerebral cavernous malformation pathogenesis.Cell death discovery · 2026Review
- Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling : EVs promote VSMC phenotypic switching.Cellular and molecular life sciences : CMLS · 2026Article
- Illuminating the Co-Phosphoregulatory Network of the Dark Kinase STK10 by Omics Approaches.BioMed research international · 2026Article
- Structural basis for MEKK2 dimerization and substrate recognition.Nature communications · 2025Article
- Phospholipase C epsilon 1 as a therapeutic target in cardiovascular diseases.Journal of advanced research · 2025Review
- Hypoglycemia Induces Diabetic Macrovascular Endothelial Dysfunction via Endothelial Cell PANoptosis, Macrophage Polarization, and VSMC Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PP2Acα Deficiency in Vascular Smooth Muscle Cells Accelerates Aortic Aneurysm and Dissection by Regulating KLF4 Phosphorylation and Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- EPSD 2.0: An Updated Database of Protein Phosphorylation Sites Across Eukaryotic Species.Genomics, proteomics & bioinformatics · 2025Article
- JOSD2 inhibits angiotensin II-induced vascular remodeling by deubiquitinating and stabilizing SMAD7.Acta pharmacologica Sinica · 2025Article
- The Role of the MAPK Signaling Pathway in Cardiovascular Disease: Pathophysiological Mechanisms and Clinical Therapy.International journal of molecular sciences · 2025Review
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
- Role of macrophages in aortic dissection pathogenesis: insights from preclinical studies to translational prospective.Science China. Life sciences · 2024Review
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Authors and funding
21 authors at 3 institutions in 1 country.
Ting-Ting Zhang *Program of Cardiovascular Research, The Eighth Affiliated Hospital (T.-T.Z., H.H., J.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0009-0006-7823-1679
Qing-Qing Lei *Department of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Jie He *Department of Cardiovascular Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong, China (J.H., X.-P.F.).ORCID 0009-0009-2487-8663
Xin Guan *Department of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Xin Zhang *Department of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0003-4914-0488
Ying HuangDepartment of Cardiology, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, China (T.-T.Z., Y.H., H.H.).
Zi-Yue ZhouDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Rui-Xin FanDepartment of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China (R.-X.F., C.-X.L.).ORCID 0000-0002-1779-2986
Ting WangDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Chen-Xi LiDepartment of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China (R.-X.F., C.-X.L.).
Jin-Yan ShangDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Zhuo-Miao LinDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Wan-Li PengDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Li-Kai XiaDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0009-0005-1320-5325
Yu-Ling HeDepartment of Pharmacology, Cardiac and Cerebrovascular Research Center (T.-T.Z., Q.-Q.L., X.G., X.Z., Z.-Y.Z., T.W., J.-Y.S., Z.-M.L., W.-L.P., L.-K.X., Y.-L.H., Z.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Chuan-Ying HongDepartment of Physiology, Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China (C.-Y.H., R.-P.P.).
Jing-Song OuDivision of Cardiac Surgery, National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases (J.-S.O.) NHC Key Laboratory of Assisted Circulation (Sun Yat-Sen University), The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Rui-Ping PangDepartment of Physiology, Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China (C.-Y.H., R.-P.P.).
Xiao-Ping FanDepartment of Cardiovascular Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong, China (J.H., X.-P.F.).ORCID 0000-0002-7067-7450
Hui HuangProgram of Cardiovascular Research, The Eighth Affiliated Hospital (T.-T.Z., H.H., J.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0001-5716-4012
Jia-Guo ZhouProgram of Cardiovascular Research, The Eighth Affiliated Hospital (T.-T.Z., H.H., J.-G.Z.), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0003-1218-7565
Sun Yat-sen University · CNGuangdong Academy of Medical Sciences · CNGuangzhou University of Chinese Medicine · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAortic dissection (AD) is a fatal cardiovascular disorder without effective medications due to unclear pathogenic mechanisms. Bestrophin3 (Best3), the predominant isoform of bestrophin family in vessels, has emerged as critical for vascular pathological processes. However, the contribution of Best3 to vascular diseases remains elusive.
methodsSmooth muscle cell-specific and endothelial cell-specific Best3 knockout mice (Best3
resultsBest3 expression in aortas of human AD samples and mouse AD models was decreased. Best3
conclusionsThese findings unveil a critical role of Best3 in regulating smooth muscle cell phenotypic switch and aortic structural integrity through controlling MEKK2/3 degradation. Best3-MEKK2/3 signaling represents a novel therapeutic target for AD.
Indexed as
Aortic DissectionMuscle, Smooth, VascularAnimalsEye ProteinsHumansMAP Kinase Signaling SystemMiceMyocytes, Smooth MusclePhosphorylationEye ProteinsVmd2L3 protein, mouseaortic dissectionMAP kinase kinase kinasesmitogen-activated protein kinasesmyocytes, smooth musclephosphorylationubiquitination
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