Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation.
Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation.
复制标题
糖尿病微血管疾病和肺纤维化：血小板和全身炎症的贡献。
DOI：
10.3390/ijms17111853
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发表时间：
2016-11-08
影响因子：
5.6
通讯作者：
Gozal E
中科院分区：
文献类型：
--
作者：
Jagadapillai R;Rane MJ;Lin X;Roberts AM;Hoyle GW;Cai L;Gozal E
糖尿病与全身性炎症和氧化应激密切相关，但其对肺血管疾病和肺功能的影响常常被忽视。多项研究在糖尿病患者和糖尿病动物模型中发现了限制性肺疾病和纤维化改变。虽然微血管功能障碍是糖尿病众所周知的并发症，但导致糖尿病诱导的肺损伤的机制在很大程度上被忽视了。我们描述了糖尿病诱导的血小板 - 内皮相互作用在持续的血管炎症和氧化损伤中可能起到的作用，这种作用导致了肺部的纤维化改变。糖尿病肺中一氧化氮合酶（NOS）激活的改变以及一氧化氮生物利用度的降低增加了血小板的激活和血管损伤，这可能是糖尿病患者中报道的血小板高反应性的原因。此外，据报道， Janus激酶/信号转导子和转录激活子（JAK/STAT）通路介导胰岛损伤，并与糖尿病的发病、炎症和血管损伤有关。许多生长因子和糖尿病诱导的激动剂通过JAK/STAT通路起作用。其他研究报道了JAK/STAT通路对肺纤维化过程的调节作用，但该通路在糖尿病肺纤维化发展中的作用尚未被考虑。这些观察结果可能为调节多种通路以减轻糖尿病的发病或其肺部后果开辟新的治疗前景。
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.
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影响因子：
7.7
作者：
Carvalho, MA;Ueno, M;Saad, MJA
通讯作者：
Saad, MJA
影响因子：
37.8
作者：
Duplain, H;Burcelin, R;Scherrer, U
通讯作者：
Scherrer, U
影响因子：
24
作者：
Ang, Lawrence;Palakodeti, Vachaspathi;Mahmud, Ehtisham
通讯作者：
Mahmud, Ehtisham
影响因子：
2.7
作者：
Dias-Junior, Carlos Alan;Cau, Stefany Bruno de Assis;Tanus-Santos, José Eduardo
通讯作者：
Tanus-Santos, José Eduardo
对糖尿病性肾病中纤维化和硬化症机制的新见解。
影响因子：
8.2
作者：
Brosius, Frank C., III
通讯作者：
Brosius, Frank C., III