Too much TRAFfic at the crossroads of diabetes and endothelial dysfunction.
Too much TRAFfic at the crossroads of diabetes and endothelial dysfunction.
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太多的交通处于糖尿病和内皮功能障碍的十字路口。
DOI：
10.1152/ajpheart.00614.2017
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Bagi,Zsolt
中科院分区：
文献类型：
--
作者：
Bagi,Zsolt
Cardiovascular complications in diabetic patients have been recognized for many decades (13) and still remain a major cause of morbidity and mortality (12, 17). Despite the advances in normalizing glucose homeostasis, the development of effective preventive therapies for diabetic vascular complications remains a major challenge (6, 9, 14, 18, 24). Considerable experimental and clinical evidence indicate that the earliest manifestation of diabetic vascular disease is the development of endothelial dysfunction (9, 10). One of the key pathologic hallmarks of endothelial dysfunction is the augmented release of endothelin-1 (ET-1). It has been established that acute or chronic elevations in glucose concentrations causes pathological changes in the function and morphology of blood vessels, which can be, in part, attributed to oxidative stress (3, 4, 8, 11, 19, 27) and activation of proinflammatory signaling pathways in vascular endothelial cells (33). While the detrimental cardiovascular effects of increased ET-1 production on vascular function and morphology are well known (7), the molecular mechanisms through which oxidative stress and proinflammatory mechanisms elicit excess endothelial production of ET-1 remain incompletely understood in the context of hyperglycemia and diabetes.Endothelin converting enzyme 1 (ECE1) is responsible for the conversion of big ET-1 to form biologically active ET-1. It is known that ECE1 can be upregulated through activation of proinflammatory signaling pathways by NF-κB and the transcription factor activator protein 1 (AP-1)(1). NF-κB and AP-1 are ubiquitously expressed transcription factors that regulate the expression of numerous genes involved in oxidative stress and immune and proinflammatory responses (21, 28). Under hyperglycemic conditions, proteasome-mediated degradation of inhibitor IκB proteins leads to NF-κB activation, which contributes to the development of diabetic microvascular complications (2). AP-1 largely contributes to the upregulation of several proinflammatory genes induced by stressactivated protein kinases, also named Jun kinases (JNKs)(25). Motivated by previous observations, the study by Padilla et al.(22) in a recent issue of the American Journal of Physiology-Heart and Circulatory Physiology set out to identify a potential upstream regulator of both NF-κB and AP-1 pathways, which could serve as a better therapeutic target in diabetes to mitigate ET-1 production in vascular endothelial cells. Findings from the study by Padilla et al. suggest that a cytoplasmic adapter molecule, TRAF3 interacting protein 2 (TRAF3IP2), plays a pivotal role in orchestrating oxidative and inflammatory activation of endothelial cells in response to high glucose concen-
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影响因子：
4.6
作者：
Bezjak，Dragica;Orellana，Nicole;Valdes，Jorge H.
通讯作者：
Valdes，Jorge H.
DOI：
10.1152/ajpheart.00478.2017
发表时间：
2018-01-01
影响因子：
4.8
作者：
Padilla, Jaume;Carpenter, Andrea J.;Chandrasekar, Bysani
通讯作者：
Chandrasekar, Bysani
影响因子：
37.8
作者：
Fox CS;Golden SH;Anderson C;Bray GA;Burke LE;de Boer IH;Deedwania P;Eckel RH;Ershow AG;Fradkin J;Inzucchi SE;Kosiborod M;Nelson RG;Patel MJ;Pignone M;Quinn L;Schauer PR;Selvin E;Vafiadis DK;American Heart Association Diabetes Committee of the Council on Lifestyle and Cardiometabolic Health, Council on Clinical Cardiology, Council on Cardiovascular and Stroke Nursing, Council on Cardiovascular Surgery and Anesthesia, Council on Quality of Care and Outcomes Research, and the American Diabetes Association
通讯作者：
American Heart Association Diabetes Committee of the Council on Lifestyle and Cardiometabolic Health, Council on Clinical Cardiology, Council on Cardiovascular and Stroke Nursing, Council on Cardiovascular Surgery and Anesthesia, Council on Quality of Care and Outcomes Research, and the American Diabetes Association
影响因子：
7.7
作者：
Park, JY;Takahara, N;King, GL
通讯作者：
King, GL
胰岛素和糖尿病。
DOI：
--
发表时间：
1986
期刊：
Transactions of the Association of American Physicians
影响因子：
--
作者：
Mako,ME;Rubenstein,AH
通讯作者：
Rubenstein,AH