AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

被引：338

作者：

He, Liyu ^{[1
]}

Wei, Qingqing ^{[2
,3
]}

Liu, Jing ^{[1
,2
,3
]}

Yi, Mixuan ^{[1
,2
,3
]}

Liu, Yu ^{[1
]}

Liu, Hong ^{[1
]}

Sun, Lin ^{[1
]}

Peng, Youming ^{[1
]}

Liu, Fuyou ^{[1
]}

Venkatachalam, Manjeri A. ^{[4
]}

Dong, Zheng ^{[1
,2
,3
]}

机构：

[1] Cent S Univ, Xiangya Hosp 2, Dept Nephrol, Changsha, Hunan, Peoples R China

[2] Augusta Univ, Med Coll Georgia, Dept Cellular Biol & Anat, 1459 Laney Walker Blvd, Augusta, GA 30912 USA

[3] Charlie Norwood VA Med Ctr, 1459 Laney Walker Blvd, Augusta, GA 30912 USA

[4] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA

来源：

KIDNEY INTERNATIONAL | 2017年 / 92卷 / 05期

基金：

美国国家卫生研究院; 中国国家自然科学基金;

关键词：

acute kidney injury; cell signaling; chronic kidney disease; fibrosis; inflammation; mitochondria; ACUTE KIDNEY INJURY; RENAL ISCHEMIA-REPERFUSION; IODINATED CONTRAST-MEDIA; TUBULAR CELL APOPTOSIS; INDUCIBLE FACTOR-I; PROXIMAL TUBULE; TGF-BETA; INTERSTITIAL FIBROSIS; OXIDATIVE STRESS; MITOCHONDRIAL BIOGENESIS;

D O I：

10.1016/j.kint.2017.06.030

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-beta, p53, hypoxia-inducible factor, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.

引用

页码：1071 / 1083

页数：13

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