| Literature DB >> 34807422 |
Noriko Miyake1, Tomoki Kosho2, Naomichi Matsumoto3.
Abstract
Ehlers-Danlos syndrome (EDS) is a genetically and clinically heterogeneous group of connective tissue disorders that typically present with skin hyperextensibility, joint hypermobility, and tissue fragility. The major cause of EDS appears to be impaired biosynthesis and enzymatic modification of collagen. In this chapter, we discuss two types of EDS that are associated with proteoglycan abnormalities: spondylodysplastic EDS and musculocontractural EDS. Spondylodysplastic EDS is caused by pathogenic variants in B4GALT7 or B3GALT6, both of which encode key enzymes that initiate glycosaminoglycan synthesis. Musculocontractural EDS is caused by mutations in CHST14 or DSE, both of which encode enzymes responsible for the post-translational biosynthesis of dermatan sulfate. The clinical and molecular characteristics of both types of EDS are described in this chapter.Entities:
Keywords: B3GALT6; B4GALT7; CHST14; DSE; Danlos syndrome (EDS); Ehlers; Glycosaminoglycan (GAG); Musculocontractural type; Proteoglycan; Spondylodysplastic type
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Year: 2021 PMID: 34807422 DOI: 10.1007/978-3-030-80614-9_10
Source DB: PubMed Journal: Adv Exp Med Biol ISSN: 0065-2598 Impact factor: 2.622