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. 2014 Aug 11;4(3):655–679. doi: 10.3390/metabo4030655

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© 2014 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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Hypotheses (H) of secondary elevation of blood KS in other MPS. H1; Accumulation of GAGs and pro-inflammatory factors induces KS synthesis. H2; GAG storage in chondrocyte leads to cell death and release of KS. H3; Accumulated HS leads to inhibition of GALNS activity. H4; Other GAGs co-deposited with KS masks the access of degradative enzymes for KS and undegraded KS is too large for filtration in kidney. H5; Fucosylation, sialyation, or sulfation modification of KS leads to resisting degradation.