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A new mechanism in the miRNA regulation of proteins leads to the binding of the miRNA directly to the DNA with premature transcriptional termination and hence the formation of truncated protein isoforms (Mxi2, Vim3). These isoforms are mediated through miRNA15a or miRNA 498, respectively. ET\u20101 can activate a cytoplasmic complex consisting of NF\u2010\u03baB p65, MAPK p38\u03b1, and PKC\u03b1. Consequently, PKC\u03b1 does not transmigrate into the nucleus, which leads to the loss of suppression of a primiRNA15a, maturation of this miRNA in the cytoplasm, tubular secretion and detectability in the urine. This mechanism has been shown in renal cell carcinoma and in proteinuric disease as a biomarker for the activation of the signalling pathway. Similarly, ET\u20101 induced miRNA 498 transmigrates into the nucleus to form the truncated protein Vim3, which is a biomarker for the benign renal cell tumour, oncocytoma. In tubulotoxicity, ET\u20101 induced miRNa133a down\u2010regulating multiple\u2010drug\u2010resistant related protein\u20102, relevant for proteinuric and cisplatin\/cyclosporine A toxicity. Current advantages and limitations of miRNAs as urinary biomarkers are discussed.<\/jats:p>","DOI":"10.1111\/boc.201800059","type":"journal-article","created":{"date-parts":[[2019,3,13]],"date-time":"2019-03-13T22:36:46Z","timestamp":1552516606000},"page":"169-186","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["MicroRNAs as markers to monitor endothelin\u20101 signalling and potential treatment in renal disease: Carcinoma \u2212 proteinuric damage \u2212 toxicity"],"prefix":"10.1111","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2054-6345","authenticated-orcid":false,"given":"Jochen W. 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