Macrophages in diabetic gastroparesis - the missing link?
Authors Neshatian L, Gibbons SJ, Farrugia G
Submitted By Gianrico Farrugia on 9/4/2014
Status Published
Journal Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
Year 2014
Date Published 8/28/2014
Volume : Pages 27 : 7 - 18
PubMed Reference 25168158
Abstract Diabetic gastroparesis results in significant morbidity for patients and major
economic burden for society. Treatment options for diabetic gastroparesis are
currently directed at symptom control rather than the underlying disease and are
limited. The pathophysiology of diabetic gastroparesis includes damage to
intrinsic and extrinsic neurons, smooth muscle, and interstitial cells of Cajal
(ICC). Oxidative damage in diabetes appears to be one of the primary insults
involved in the pathogenesis of several complications of diabetes, including
gastroparesis. Recent studies have highlighted the potential role of macrophages
as key cellular elements in the pathogenesis of diabetic gastroparesis.
Macrophages are important for both homeostasis and defense against a variety of
pathogens. Heme oxygenase 1 (HO1), an enzyme expressed in a subset of
macrophages has emerged as a major protective mechanism against oxidative
stress. Activation of macrophages with high levels of HO1 expression protects
against development of delayed gastric emptying in animal models of diabetes,
while activation of macrophages that do not express HO1 are linked to
neuromuscular cell injury. Targeting macrophages and HO1 may therefore be a
therapeutic option in diabetic gastroparesis.


Investigators with authorship
NameInstitution
Gianrico FarrugiaMayo Clinic Rochester

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