ELABELA and an ELABELA fragment protect against AKI

Hong Chen, Lin Wang, Wenjun Wang, Cheng Cheng, Yu Zhang, Yu Zhou, Congyi Wang, Xiaoping Miao, Jiao Wang, Chao Wang, Jianshuang Li, Ling Zheng, Kun Huang

Research output: Contribution to journalArticlepeer-review

109 Scopus citations


Renal ischemia-reperfusion (I/R) injury is the most common cause of AKI, which associates with high mortality and has no effective therapy. ELABELA (ELA) is a newly identified 32-residue hormone peptide highly expressed in adult kidney. To investigate whether ELA has protective effects on renal I/R injury, we administered the mature peptide (ELA32) or the 11-residue furin-cleaved fragment (ELA11) to hypoxia-reperfusion (H/R)-injured or adriamycin-treated renal tubular cells in vitro. ELA32 and ELA11 significantly inhibited the elevation of the DNA damage response, apoptosis, and inflammation in H/R-injured renal tubular cells and suppressed adriamycin-induced DNA damage response. Similarly, overexpression of ELA32 or ELA11 significantly inhibited H/R-induced cell death, DNA damage response, and inflammation. Notably, treatment of mice with ELA32 or ELA11 but not an ELA11 mutant with a cysteine to alanine substitution at the N terminus (AE11C) inhibited I/R injury-induced renal fibrosis, inflammation, apoptosis, and the DNA damage response and markedly reduced the renal tubular lesions and renal dysfunction. Together, our results suggest that ELA32 and ELA11 may be therapeutic candidates for treating AKI.

Original languageEnglish
Pages (from-to)2694-2707
Number of pages14
JournalJournal of the American Society of Nephrology
Issue number9
StatePublished - Sep 2017


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