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Glycoproteins in Degenerative Disease and Xenograft Rejection

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Glycoproteins and Human Disease

Abstract

Aconsiderable proportion of degenerative diseases is age-related. Advanced protein glycosylation increases with age and involves nonenzymatic covalent addition of carbohydrate to tissue proteins, and is a prominent feature of disorders affecting the normal biological functions of connective tissue, lens, blood vessels and nerves. In diabetes, tissue damage occurs over much shorter time periods than in normal individuals; thus, experimental studies have focused on diabetic models since the lesions are similar to those of old age.1 Advanced glycation end products modify structures and functions of the extracellular matrix, cell surface molecules including vitronectin, laminin, lens crystallin and collagens2 and may promote a generalized form of vasculopathy.3 Gangliosides have also been found to accumulate in senile cataracts; among them, sialyl-Lex neolacto-series gangliosides have been identified.4

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© 1997 Springer-Verlag Berlin Heidelberg

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Brockhausen, I., Kuhns, W. (1997). Glycoproteins in Degenerative Disease and Xenograft Rejection. In: Glycoproteins and Human Disease. Medical Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-21960-7_18

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  • DOI: https://doi.org/10.1007/978-3-662-21960-7_18

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-21962-1

  • Online ISBN: 978-3-662-21960-7

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