Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

The endothelial border to health: Mechanistic evidence of the hyperglycemic culprit of inflammatory disease acceleration

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Managerial strategies and policies - Analysis of patient satisfaction based on demographic data

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. The influence of digital media on the success of a health care unit

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Why epidemiological and clinical intervention studies often give different or diverging results?

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. CGRP in rat mesenteric artery and vein - receptor expression, CGRP presence and potential roles

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Fluorescent Analogues of Human α-Calcitonin Gene-Related Peptide with Potent Vasodilator Activity

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. The Microbiotic Highway to Health-New Perspective on Food Structure, Gut Microbiota, and Host Inflammation

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

Vis graf over relationer

The endothelial cell (EC) layer constitutes a barrier that controls movements of fluid, solutes and cells between blood and tissue. Further, the endothelial layer regulates vascular tone and directs local humoral and cellular inflammatory processes. The strategic position makes it an important player for maintenance of health and for development of a number of diseases. Endothelial dysfunction is known to be an important component of type 2 diabetes, but is also assumed to be involved in many other diseases, for example, rheumatoid arthritis, inflammatory bowel disease, asthma, and cardiovascular diseases. We here suggest that the EC plays a pivotal role in disease pathophysiology through initiation, potentiation, and maintenance of several inflammatory mechanisms. Our contention is based on the observation that hyperglycemia-intermittent or sustained, local or systemic-is a major culprit for several endothelial dysfunctions. There is also mounting epidemiological evidence that dietary intake of refined sugars is important for the development of a number of diseases beyond obesity and type 2 diabetes. Various diseases involving inflammatory and immunological components are accelerated by hyperglycemic events because the endothelium transduces "high glucose" signaling into significant pathophysiological phenomena leading to reduced endothelial barrier function, compromised vascular tone regulation and inflammation (e.g., cytokine secretion and RAGE activation). In addition, endothelial extracellular proteins form epitopes for potential specific antibody formation upon interactions with reducing sugars. This paper reviews the endothelial metabolism, biology, inflammatory processes, physical barrier functions, and summarizes evidence that although stochastic in nature, endothelial responses to hyperglycemia are major contributors to disease pathophysiology. We present molecular and mechanistic evidence that both biological and physical barriers, protein function, specific immunity, and inflammatory processes are compromised by hyperglycemic events and thus, hyperglycemic events alone should be considered risk factors for numerous human diseases. © 2017 IUBMB Life, 69(3):148-161, 2017.

OriginalsprogEngelsk
TidsskriftIUBMB Life
Vol/bind69
Udgave nummer3
Sider (fra-til)148-161
Antal sider14
ISSN1521-6543
DOI
StatusUdgivet - mar. 2017

ID: 50175272