Consequences of Both Coxsackievirus B4 and Type 1 Diabetes on Female Non-Obese Diabetic Mouse Kidneys.
Consequences of Both Coxsackievirus B4 and Type 1 Diabetes on Female Non-Obese Diabetic Mouse Kidneys.
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DOI：
10.3390/microorganisms9112357
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发表时间：
2021-11-15
期刊：
影响因子：
4.5
通讯作者：
Coschigano KT
中科院分区：
文献类型：
--
作者：
Walter DL;Thuma JR;Malgor R;Schwartz FL;McCall KD;Coschigano KT
尽管2019年颁布了关于推进美国肾脏健康倡议的行政命令，但肾脏疾病已经从美国的第9位死亡原因上升到第8位。肾脏病学领域最近的一个进展是确定与肾脏疾病过程或损伤有关的分子标记和/或分子谱，这些标记和/或分子谱可以帮助确定损伤的原因并预测患者的预后。虽然这些研究取得了一定的成功，但他们还没有考虑到许多导致肾脏疾病的健康状况（糖尿病、高血压等）也可能由环境因素（如病毒）引起，而环境因素本身也可能导致肾脏疾病。因此，本研究的目的是确定可以区分糖尿病（导致肾脏疾病的健康状况）和柯萨奇病毒B4 （CVB4）暴露（可导致糖尿病和/或肾脏疾病）引起的肾损伤的分子和表型特征，无论是单独还是共同。由于非肥胖糖尿病（NOD）小鼠对1型糖尿病（T1D）和cvb4介导的肾损伤都很敏感，因此研究人员将其用于本研究，以便更好地了解高血糖和病毒暴露在单独或联合发生时如何改变肾脏的分子和表型。虽然没有观察到肾功能的变化，但基于T1D和CVB4单独或共同暴露，肾脏损伤的分子生物标志物显着上调和下调，但没有可预测的模式。通过将个体生物标志物与功能和表型测量（即尿白蛋白肌酐比、血清肌酐、肾脏重量和体重）相结合，我们能够根据损伤类型对损伤组进行无偏分离。这项研究提供了证据，证明肾脏疾病健康状况下独特的肾损伤概况是可识别的，并将帮助我们在未来确定肾损伤的原因。
Despite the 2019 Executive Order on Advancing American Kidney Health Initiative, kidney disease has moved up in rank from the 9th to the 8th leading cause of death in the United States. A recent push in the field of nephrology has been to identify molecular markers and/or molecular profiles involved in kidney disease process or injury that can help identify the cause of injury and predict patient outcomes. While these studies have had moderate success, they have not yet considered that many of the health conditions that cause kidney disease (diabetes, hypertension, etc.) can also be caused by environmental factors (such as viruses), which in and of themselves can cause kidney disease. Thus, the goal of this study was to identify molecular and phenotypic profiles that can differentiate kidney injury caused by diabetes (a health condition resulting in kidney disease) and coxsackievirus B4 (CVB4) exposure (which can cause diabetes and/or kidney disease), both alone and together. Non-obese diabetic (NOD) mice were used for this study due to their susceptibility to both type 1 diabetes (T1D)- and CVB4-mediated kidney injury, in order to glean a better understanding of how hyperglycemia and viral exposure, when occurring on their own and in combination, may alter the kidneys’ molecular and phenotypic profiles. While no changes in kidney function were observed, molecular biomarkers of kidney injury were significantly up- and downregulated based on T1D and CVB4 exposure, both alone and together, but not in a predictable pattern. By combining individual biomarkers with function and phenotypic measurements (i.e., urinary albumin creatinine ratio, serum creatinine, kidney weight, and body weight), we were able to perform an unbiased separation of injury group based on the type of injury. This study provides evidence that unique kidney injury profiles within a kidney disease health condition are identifiable, and will help us to identify the causes of kidney injury in the future.
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影响因子：
2.2
作者：
Khan, Fatima Abid;Fatima, Syeda Sadia;Shahid, Sana
通讯作者：
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影响因子：
3.9
作者：
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1型糖尿病的病毒触发因素：利弊。
影响因子：
7.7
作者：
Filippi, Christophe M.;von Herrath, Matthias G.
通讯作者：
von Herrath, Matthias G.
影响因子：
1.4
作者：
Coschigano, K. T.;Wetzel, A. N.;Kopchick, J. J.
通讯作者：
Kopchick, J. J.
影响因子：
6.7
作者：
Cheng J;Ke Q;Jin Z;Wang H;Kocher O;Morgan JP;Zhang J;Crumpacker CS
通讯作者：
Crumpacker CS