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How high glucose levels affect tendon homeostasis


Snedeker, J G (2016). How high glucose levels affect tendon homeostasis. In: Ackermann, P W; Hart, D A. Metabolic Influences on Risk for Tendon Disorders. Cham: Springer, 191-198.

Abstract

Among the many factors playing a role in tendon disease, unregulated biochemical reactions between glucose and the collagen extracellular matrix are coming increasingly into focus. We have shown that formation of advanced glycation end-products that cross-link the collagen extracellular matrix can drastically affect cellular level mechanical properties of the matrix, and in turn affect cell-level biomechanical stimuli during physiological loading of the tissue. We suggest that these may adversely affect tendon cell response to matrix damage, as well as the quality of the consequent repair. If such mechanical feedback loops are altered, the ability of tendon cells to maintain tissue in a functional, healthy state may be compromised. Although key foundational elements of biochemical, biomechanical, and biological understanding are now in place, the full extent of how these aspects interact, including the precise mechanisms by which advanced glycation end-products pathologically disrupt connective tissue homeostasis and damage repair, are only beginning to be adequately appreciated.

Abstract

Among the many factors playing a role in tendon disease, unregulated biochemical reactions between glucose and the collagen extracellular matrix are coming increasingly into focus. We have shown that formation of advanced glycation end-products that cross-link the collagen extracellular matrix can drastically affect cellular level mechanical properties of the matrix, and in turn affect cell-level biomechanical stimuli during physiological loading of the tissue. We suggest that these may adversely affect tendon cell response to matrix damage, as well as the quality of the consequent repair. If such mechanical feedback loops are altered, the ability of tendon cells to maintain tissue in a functional, healthy state may be compromised. Although key foundational elements of biochemical, biomechanical, and biological understanding are now in place, the full extent of how these aspects interact, including the precise mechanisms by which advanced glycation end-products pathologically disrupt connective tissue homeostasis and damage repair, are only beginning to be adequately appreciated.

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Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:04 Faculty of Medicine > Balgrist University Hospital, Swiss Spinal Cord Injury Center
Dewey Decimal Classification:610 Medicine & health
Uncontrolled Keywords:Advanced glycation endproduct; Aging; Biomechanics; Diabetes; Mechanobiology
Language:English
Date:1 January 2016
Deposited On:02 Feb 2017 10:38
Last Modified:02 Feb 2018 11:58
Publisher:Springer
Series Name:Advances in Experimental Medicine and Biology
Number:920
ISSN:0065-2598
ISBN:978-3-319-33943-6
OA Status:Closed
Publisher DOI:https://doi.org/10.1007/978-3-319-33943-6_18
PubMed ID:27535261

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