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Int. J. Mol. Sci. 2016, 17(11), 1853; doi:10.3390/ijms17111853

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

1
Department of Pediatrics, School of Medicine, University of Louisville, Louisville, KY 40292, USA
2
Medicine/Nephrology, School of Medicine, University of Louisville, Louisville, KY 40292, USA
3
Biochemistry and Molecular Biology, School of Medicine, University of Louisville, Louisville, KY 40292, USA
4
Department of Thoracic Surgery, the First Hospital of Jilin University, Changchun 130021, China
5
Physiology, School of Medicine, University of Louisville, Louisville, KY 40292, USA
6
Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY 40292, USA
7
Pharmacology & Toxicology, School of Medicine, University of Louisville, Louisville, KY 40292, USA
8
Radiation Oncology, School of Medicine, University of Louisville, Louisville, KY 40292, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Joseph V. Moxon
Received: 6 September 2016 / Revised: 24 October 2016 / Accepted: 1 November 2016 / Published: 8 November 2016
(This article belongs to the Special Issue Diabetic Complications: Pathophysiology, Mechanisms, and Therapies)
View Full-Text   |   Download PDF [1143 KB, uploaded 8 November 2016]   |  

Abstract

Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS) activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences. View Full-Text
Keywords: lung fibrosis; endothelial injury; platelet; nitric oxide; JAK/STAT lung fibrosis; endothelial injury; platelet; nitric oxide; JAK/STAT
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MDPI and ACS Style

Jagadapillai, R.; Rane, M.J.; Lin, X.; Roberts, A.M.; Hoyle, G.W.; Cai, L.; Gozal, E. Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation. Int. J. Mol. Sci. 2016, 17, 1853.

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