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Tubular overexpression of Gremlin in transgenic mice aggravates renal damage in diabetic nephropathy.在转基因小鼠中,Gremlin在肾小管中的过表达会加重糖尿病肾病中的肾损伤。
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Novel mechanism of transcriptional regulation of cell matrix protein through CREB.通过CREB对细胞基质蛋白进行转录调控的新机制。
Cell Cycle. 2015;14(16):2598-608. doi: 10.1080/15384101.2015.1064204. Epub 2015 Jun 26.
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Muscle wasting in disease: molecular mechanisms and promising therapies.疾病导致的肌肉减少症:分子机制和有前途的治疗方法。
Nat Rev Drug Discov. 2015 Jan;14(1):58-74. doi: 10.1038/nrd4467.
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Multiple mechanisms in renal artery stenosis-induced renal interstitial fibrosis.肾动脉狭窄诱导肾间质纤维化的多种机制。
Nephron Exp Nephrol. 2014;128(1-2):57-66. doi: 10.1159/000366481. Epub 2014 Nov 8.
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Tuberin-deficiency downregulates N-cadherin and upregulates vimentin in kidney tumor of TSC patients.结节性硬化症患者肾肿瘤中,结节蛋白缺乏会下调N-钙黏蛋白并上调波形蛋白。
Oncotarget. 2014 Aug 30;5(16):6936-46. doi: 10.18632/oncotarget.2206.
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Emerging urinary markers of renal injury in obstructive nephropathy.梗阻性肾病中肾脏损伤的新型尿液标志物。
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Tuberin in renal cell hypertrophy.肾细胞肥大中的结节性硬化蛋白
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8
Alterations in tubular epithelial cells in diabetic nephropathy.糖尿病肾病中肾小管上皮细胞的改变。
J Nephrol. 2013 Sep-Oct;26(5):865-9. doi: 10.5301/jn.5000287. Epub 2013 Aug 6.
9
Tuberin inhibits production of the matrix protein fibronectin in diabetes.结节性硬化症蛋白可抑制糖尿病细胞外基质蛋白纤维连接蛋白的产生。
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10
Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.糖尿病疾病模型中的肾功能:糖尿病肾脏病理生理学中的管状系统。
Annu Rev Physiol. 2012;74:351-75. doi: 10.1146/annurev-physiol-020911-153333.

糖尿病中的肾脏萎缩与肥大:哪些细胞参与其中?

Kidney atrophy vs hypertrophy in diabetes: which cells are involved?

机构信息

a Department of Geriatric, Geriatric Research, Education, and Clinical Center , South Texas Veterans Healthcare System , San Antonio , TX.

b Department of Cell Systems and Anatomy , University of Texas Health Science Center at San Antonio , San Antonio , TX.

出版信息

Cell Cycle. 2018;17(14):1683-1687. doi: 10.1080/15384101.2018.1496744. Epub 2018 Jul 30.

DOI:10.1080/15384101.2018.1496744
PMID:29995580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6133324/
Abstract

One of the first structural changes in diabetic nephropathy (DN) is the renal enlargement. These changes resulted in renal hypertrophy in both glomerular and tubular cells. Shrink in the kidney size, which described as kidney atrophy resulted from the loss of nephrons or abnormal nephron function and lead to loss of the kidney function. On the other hand, increase in kidney size, which described as hypertrophy resulted from increase in proximal tubular epithelial and glomerular cells size. However overtime, tubular atrophy and tubulointerstitial fibrosis occurs as subsequent changes in tubular cell hypertrophy, which is associated with the infiltration of fibroblast cells into the tubulointerstitial space. The rate of deterioration of kidney function shows a strong correlation with the degree of tubulointerstitial fibrosis. A consequence of long-standing diabetes/hyperglycemia may lead to major changes in renal structure that occur but not specific only to nephropathy. Identifying type of cells that involves in renal atrophy and hypertrophy may help to find a therapeutic target to treat diabetic nephropathy. In summary, the early changes in diabetic kidney are mainly includes the increase in tubular basement membrane thickening which lead to renal hypertrophy. On the other hand, only renal tubule is subjected to apoptosis, which is one of the characteristic morphologic changes in diabetic kidney to form tubular atrophy at the late stage of diabetes.

摘要

糖尿病肾病(DN)的最早结构变化之一是肾脏增大。这些变化导致肾小球和肾小管细胞都发生肾肥大。肾脏大小的缩小,即肾萎缩,是由于肾小球或肾小管功能异常导致肾单位丢失而引起的,会导致肾功能丧失。另一方面,肾脏大小的增加,即肥大,是由于近端肾小管上皮细胞和肾小球细胞大小的增加所致。然而,随着时间的推移,肾小管萎缩和肾小管间质纤维化会发生,这是肾小管细胞肥大的后续变化,与成纤维细胞浸润到肾小管间质空间有关。肾功能恶化的速度与肾小管间质纤维化的程度有很强的相关性。长期糖尿病/高血糖可能导致肾脏结构发生重大变化,但不仅限于肾病。确定参与肾萎缩和肥大的细胞类型可能有助于找到治疗糖尿病肾病的治疗靶点。总之,糖尿病肾脏的早期变化主要包括肾小管基底膜增厚导致的肾肥大。另一方面,只有肾小管发生细胞凋亡,这是糖尿病肾脏的特征性形态学变化之一,在糖尿病晚期形成肾小管萎缩。