Abstract:
AIMS:The risk factors promoting acute kidney injury (AKI) to chronic kidney disease (CKD) progression remain largely unknown. The aim of the present study was to investigate whether hyperhomocysteinemia (Hhcy) accelerates the development of renal fibrosis after AKI. RESULTS:Hhcy aggravated ischemia-reperfusion-induced AKI and the subsequent development of renal fibrotic lesions characterized by excessive extracellular matrix deposition. Mechanistically, the RNA binding protein human antigen R (HuR) bound to the 3'-untranslated region (3'-UTR) of heme oxygenase-1 (HO-1) messenger RNA (mRNA). Homocysteine (Hcy) downregulated HuR expression, reduced the binding of HuR to the 3'-UTR of HO-1, and thereafter decreased HO-1 expression. Administration of the HO-1 inducer cobalt protoporphyrin-IX significantly hindered Hhcy-augmented reactive oxygen species production and renal fibrotic lesions. Innovation and Conclusion: These data indicate that Hhcy might be a novel risk factor that promotes AKI to CKD progression. Lowering Hcy level or HO-1 induction might be a potential therapeutic strategy to improve the outcome of AKI.
journal_name
Antioxid Redox Signaljournal_title
Antioxidants & redox signalingauthors
Li S,Qiu B,Lu H,Lai Y,Liu J,Luo J,Zhu F,Hu Z,Zhou M,Tian J,Zhou Z,Yu S,Yi F,Nie Jdoi
10.1089/ars.2017.7397subject
Has Abstractpub_date
2019-05-01 00:00:00pages
1635-1650issue
13eissn
1523-0864issn
1557-7716journal_volume
30pub_type
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