English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury (AKI). Non-coding RNAs are crucially involved in its pathophysiology. We identified hypoxia-induced long non-coding RNA  Malat1  (Metastasis Associated Lung Adenocarcinoma Transcript 1) to be upregulated in renal I/R injury. We here elucidated the functional role of  Malat1 in vitro  and its potential contribution to kidney injury  in vivo .  Malat1  was upregulated in kidney biopsies and plasma of patients with AKI, in murine hypoxic kidney tissue as well as in cultured and  ex vivo  sorted hypoxic endothelial cells and tubular epithelial cells.  Malat1  was transcriptionally activated by hypoxia-inducible factor 1-α.  In vitro ,  Malat1  inhibition reduced proliferation and the number of endothelial cells in the S-phase of the cell cycle.  In vivo ,  Malat1  knockout and wildtype mice showed similar degrees of outer medullary tubular epithelial injury, proliferation, capillary rarefaction, inflammation and fibrosis, survival and kidney function. Small-RNA sequencing and whole genome expression analysis revealed only minor changes between ischemic  Malat1  knockout and wildtype mice. Contrary to previous studies, which suggested a prominent role of  Malat1  in the induction of disease, we did not confirm an  in vivo  role of  Malat1  concerning renal I/R-injury.

Hypoxia-induced long non-coding RNA Malat1 is dispensable for renal ischemia/reperfusion-injury