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糖尿病肾病中系膜扩张的病理生理学:系膜结构、肾小球生物力学以及生化信号传导与调节

Pathophysiology of mesangial expansion in diabetic nephropathy: mesangial structure, glomerular biomechanics, and biochemical signaling and regulation.

作者信息

Thomas Haryana Y, Ford Versypt Ashlee N

机构信息

Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Buffalo, NY, USA.

Institute for Computational and Data Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA.

出版信息

J Biol Eng. 2022 Aug 2;16(1):19. doi: 10.1186/s13036-022-00299-4.

Abstract

Diabetic nephropathy, a kidney complication arising from diabetes, is the leading cause of death in diabetic patients. Unabated, the growing epidemic of diabetes is increasing instances of diabetic nephropathy. Although the main causes of diabetic nephropathy have been determined, the mechanisms of their combined effects on cellular and tissue function are not fully established. One of many damages of diabetic nephropathy is the development of fibrosis within the kidneys, termed mesangial expansion. Mesangial expansion is an important structural lesion that is characterized by the aberrant proliferation of mesangial cells and excess production of matrix proteins. Mesangial expansion is involved in the progression of kidney failure in diabetic nephropathy, yet its causes and mechanism of impact on kidney function are not well defined. Here, we review the literature on the causes of mesangial expansion and its impacts on cell and tissue function. We highlight the gaps that still remain and the potential areas where bioengineering studies can bring insight to mesangial expansion in diabetic nephropathy.

摘要

糖尿病肾病是糖尿病引发的一种肾脏并发症,是糖尿病患者死亡的主要原因。糖尿病流行趋势愈演愈烈,糖尿病肾病的发病例数也随之增加。尽管糖尿病肾病的主要病因已被确定,但其综合作用于细胞和组织功能的机制尚未完全明确。糖尿病肾病的诸多损害之一是肾脏内出现纤维化,即系膜扩张。系膜扩张是一种重要的结构病变,其特征是系膜细胞异常增殖和基质蛋白过度产生。系膜扩张参与了糖尿病肾病肾衰竭的进展,但其病因及其对肾功能的影响机制尚不清楚。在此,我们综述了关于系膜扩张的原因及其对细胞和组织功能影响的文献。我们强调了仍然存在的差距以及生物工程研究可以为糖尿病肾病系膜扩张带来见解的潜在领域。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e3/9347079/db01cfd1d69e/13036_2022_299_Fig1_HTML.jpg

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