The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update

被引：85

作者：

Wu, Tong ^{[1
]}

Ding, Lei ^{[1
]}

Andoh, Vivian ^{[2
]}

Zhang, Jiaxin ^{[1
]}

Chen, Liang ^{[1
]}

机构：

[1] Jiangsu Univ, Sch Life Sci, Zhenjiang 212013, Peoples R China

[2] Jiangsu Univ, Sch Food Sci & Biol Engn, Zhenjiang 212013, Peoples R China

来源：

LIFE-BASEL | 2023年 / 13卷 / 02期

基金：

中国国家自然科学基金;

关键词：

diabetic nephropathy; hyperglycemia; mechanism; renal cell injury; PROTEIN-KINASE-C; GLYCATION END-PRODUCTS; GROWTH-FACTOR-BETA; TO-MESENCHYMAL TRANSITION; HIGH GLUCOSE-LEVELS; MESANGIAL CELLS; GENE-EXPRESSION; POLYOL PATHWAY; PATHOGENETIC MECHANISMS; PODOCYTE DYSFUNCTION;

D O I：

10.3390/life13020539

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Diabetic Nephropathy (DN) is a serious complication of type I and II diabetes. It develops from the initial microproteinuria to end-stage renal failure. The main initiator for DN is chronic hyperglycemia. Hyperglycemia (HG) can stimulate the resident and non-resident renal cells to produce humoral mediators and cytokines that can lead to functional and phenotypic changes in renal cells and tissues, interference with cell growth, interacting proteins, advanced glycation end products (AGEs), etc., ultimately resulting in glomerular and tubular damage and the onset of kidney disease. Therefore, poor blood glucose control is a particularly important risk factor for the development of DN. In this paper, the types and mechanisms of DN cell damage are classified and summarized by reviewing the related literature concerning the effect of hyperglycemia on the development of DN. At the cellular level, we summarize the mechanisms and effects of renal damage by hyperglycemia. This is expected to provide therapeutic ideas and inspiration for further studies on the treatment of patients with DN.

引用

页数：18

共 148 条

[1] Bioenergetic characterization of mouse podocytes [J].

Abe, Yoshifusa ;

Sakairi, Toru ;

Kajiyama, Hiroshi ;

Shrivastav, Shashi ;

Beeson, Craig ;

Kopp, Jeffrey B. .

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2010, 299 (02) :C464-C476

[2] Diabetic Kidney Disease Challenges, Progress, and Possibilities [J].

Alicic, Radica Z. ;

Rooney, Michele T. ;

Tuttle, Katherine R. .

CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2017, 12 (12) :2032-2045

[3] Molecular mechanisms in the pathogenesis of diabetic nephropathy: An update [J].

Arora, Mandeep Kumar ;

Singh, Umesh Kumar .

VASCULAR PHARMACOLOGY, 2013, 58 (04) :259-271

[4] Pathophysiology of Diabetic Nephropathy: Involvement of Multifaceted Signalling Mechanism [J].

Balakumar, Pitchai ;

Arora, Mandeep Kumar ;

Reddy, Jayarami ;

Anand-Srivastava, Madhu B. .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2009, 54 (02) :129-138

[5] Apoptosis of tubular epithelial cells in glycogen nephrosis during diabetes [J].

Bamri-Ezzine, S ;

Ao, ZJ ;

Londoño, I ;

Gingras, D ;

Bendayan, M .

LABORATORY INVESTIGATION, 2003, 83 (07) :1069-1080

[6] THE EFFECT OF OXIDATION ON SORBITOL PATHWAY KINETICS [J].

BARNETT, PA ;

GONZALEZ, RG ;

CHYLACK, LT ;

CHENG, HM .

DIABETES, 1986, 35 (04) :426-432

[7] Protein kinase C and phospholipase D: intimate interactions in intracellular signaling [J].

Becker, KP ;

Hannun, YA .

CELLULAR AND MOLECULAR LIFE SCIENCES, 2005, 62 (13) :1448-1461

[8] DEVELOPMENTAL AND PHYSIOLOGICAL REGULATION OF ALDOSE REDUCTASE MESSENGER-RNA EXPRESSION IN RENAL MEDULLA [J].

BONDY, CA ;

LIGHTMAN, SL ;

LIGHTMAN, SL .

MOLECULAR ENDOCRINOLOGY, 1989, 3 (09) :1409-1416

[9] Glucose scavenging of nitric oxide [J].

Brodsky, SV ;

Morrishow, AM ;

Dharia, N ;

Gross, SS ;

Goligorsky, MS .

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2001, 280 (03) :F480-F486

[10] Biochemistry and molecular cell biology of diabetic complications [J].

Brownlee, M .

NATURE, 2001, 414 (6865) :813-820

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