| Literature DB >> 28890325 |
Liyu He1, Qingqing Wei2, Jing Liu3, Mixuan Yi3, Yu Liu1, Hong Liu1, Lin Sun1, Youming Peng1, Fuyou Liu1, Manjeri A Venkatachalam4, Zheng Dong5.
Abstract
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-β, 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.Entities:
Keywords: acute kidney injury; cell signaling; chronic kidney disease; fibrosis; inflammation; mitochondria
Mesh:
Substances:
Year: 2017 PMID: 28890325 PMCID: PMC5683166 DOI: 10.1016/j.kint.2017.06.030
Source DB: PubMed Journal: Kidney Int ISSN: 0085-2538 Impact factor: 10.612