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Arterial tortuosity syndrome : an ascorbate compartmentalization disorder?

(2021) ANTIOXIDANTS & REDOX SIGNALING. 34(11). p.875-889
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Abstract
Critical Issues: Although several hypotheses have been forwarded, the molecular mechanisms linking disrupted GLUT10 activity with arterial malformations are largely unknown. Recent Advances: The vascular and systemic manifestations and natural history of ATS patients have been largely delineated. GLUT10 was identified as an intracellular transporter of dehydroascorbic acid, which contributes to collagen and elastin cross-linking in the endoplasmic reticulum, redox homeostasis in the mitochondria, and global and gene-specific methylation/hydroxymethylation affecting epigenetic regulation in the nucleus. We revise here the current knowledge on ATS and the role of GLUT10 within the compartmentalization of ascorbate in physiological and diseased states. Future Directions: Centralization of clinical, treatment, and outcome data will enable better management for ATS patients. Establishment of representative animal disease models could facilitate the study of pathomechanisms underlying ATS. This might be relevant for other forms of vascular dysplasia, such as isolated aneurysm formation, hypertensive vasculopathy, and neovascularization. Antioxid. Redox Signal. 00, 000-000.
Keywords
arterial tortuosity syndrome, ascorbate, GLUT10, compartmentalization, GLUCOSE-TRANSPORTER, VITAMIN-C, AORTIC-ANEURYSM, OXIDATIVE STRESS, GLUT-FAMILY, DEFICIENCY LEADS, ISCHEMIC-STROKE, SLC2A10 GENE, ACID, MUTATIONS

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MLA
Boel, Annekatrien, et al. “Arterial Tortuosity Syndrome : An Ascorbate Compartmentalization Disorder?” ANTIOXIDANTS & REDOX SIGNALING, vol. 34, no. 11, 2021, pp. 875–89, doi:10.1089/ars.2019.7843.
APA
Boel, A., Veszelyi, K., Nemeth, C. E., Beyens, A., Willaert, A., Coucke, P., … Margittai, E. (2021). Arterial tortuosity syndrome : an ascorbate compartmentalization disorder? ANTIOXIDANTS & REDOX SIGNALING, 34(11), 875–889. https://doi.org/10.1089/ars.2019.7843
Chicago author-date
Boel, Annekatrien, Krisztina Veszelyi, Csilla E. Nemeth, Aude Beyens, Andy Willaert, Paul Coucke, Bert Callewaert, and Eva Margittai. 2021. “Arterial Tortuosity Syndrome : An Ascorbate Compartmentalization Disorder?” ANTIOXIDANTS & REDOX SIGNALING 34 (11): 875–89. https://doi.org/10.1089/ars.2019.7843.
Chicago author-date (all authors)
Boel, Annekatrien, Krisztina Veszelyi, Csilla E. Nemeth, Aude Beyens, Andy Willaert, Paul Coucke, Bert Callewaert, and Eva Margittai. 2021. “Arterial Tortuosity Syndrome : An Ascorbate Compartmentalization Disorder?” ANTIOXIDANTS & REDOX SIGNALING 34 (11): 875–889. doi:10.1089/ars.2019.7843.
Vancouver
1.
Boel A, Veszelyi K, Nemeth CE, Beyens A, Willaert A, Coucke P, et al. Arterial tortuosity syndrome : an ascorbate compartmentalization disorder? ANTIOXIDANTS & REDOX SIGNALING. 2021;34(11):875–89.
IEEE
[1]
A. Boel et al., “Arterial tortuosity syndrome : an ascorbate compartmentalization disorder?,” ANTIOXIDANTS & REDOX SIGNALING, vol. 34, no. 11, pp. 875–889, 2021.
@article{8706614,
  abstract     = {{Critical Issues: Although several hypotheses have been forwarded, the molecular mechanisms linking disrupted GLUT10 activity with arterial malformations are largely unknown. Recent Advances: The vascular and systemic manifestations and natural history of ATS patients have been largely delineated. GLUT10 was identified as an intracellular transporter of dehydroascorbic acid, which contributes to collagen and elastin cross-linking in the endoplasmic reticulum, redox homeostasis in the mitochondria, and global and gene-specific methylation/hydroxymethylation affecting epigenetic regulation in the nucleus. We revise here the current knowledge on ATS and the role of GLUT10 within the compartmentalization of ascorbate in physiological and diseased states. Future Directions: Centralization of clinical, treatment, and outcome data will enable better management for ATS patients. Establishment of representative animal disease models could facilitate the study of pathomechanisms underlying ATS. This might be relevant for other forms of vascular dysplasia, such as isolated aneurysm formation, hypertensive vasculopathy, and neovascularization. Antioxid. Redox Signal. 00, 000-000.}},
  author       = {{Boel, Annekatrien and Veszelyi, Krisztina and Nemeth, Csilla E. and Beyens, Aude and Willaert, Andy and Coucke, Paul and Callewaert, Bert and Margittai, Eva}},
  issn         = {{1523-0864}},
  journal      = {{ANTIOXIDANTS & REDOX SIGNALING}},
  keywords     = {{arterial tortuosity syndrome,ascorbate,GLUT10,compartmentalization,GLUCOSE-TRANSPORTER,VITAMIN-C,AORTIC-ANEURYSM,OXIDATIVE STRESS,GLUT-FAMILY,DEFICIENCY LEADS,ISCHEMIC-STROKE,SLC2A10 GENE,ACID,MUTATIONS}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{875--889}},
  title        = {{Arterial tortuosity syndrome : an ascorbate compartmentalization disorder?}},
  url          = {{http://dx.doi.org/10.1089/ars.2019.7843}},
  volume       = {{34}},
  year         = {{2021}},
}

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