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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:p>\n                    <jats:italic>APOL1<\/jats:italic>\n                    risk variants are associated with increased risk of kidney disease in patients of African ancestry, but not all individuals with the\n                    <jats:italic>APOL1<\/jats:italic>\n                    high-risk genotype develop kidney disease. As APOL1 gene expression correlates closely with the degree of kidney cell injury in both cell and animal models, the mechanisms regulating APOL1 expression may be critical determinants of risk allele penetrance. The APOL1 messenger RNA includes Alu elements at the 3\u2032 untranslated region that can form a double-stranded RNA structure (Alu-dsRNA) susceptible to posttranscriptional adenosine deaminase acting on RNA (ADAR)\u2013mediated adenosine-to-inosine (A-to-I) editing, potentially impacting gene expression. We studied the effects of ADAR expression and A-to-I editing on APOL1 levels in podocytes, human kidney tissue, and a transgenic APOL1 mouse model. In interferon-\u03b3 (IFN-\u03b3)\u2013stimulated human podocytes, ADAR down-regulates APOL1 by preventing melanoma differentiation-associated protein 5 (MDA5) recognition of dsRNA and the subsequent type I interferon (IFN-I) response. Knockdown experiments showed that recognition of APOL1 messenger RNA itself is an important contributor to the MDA5-driven IFN-I response. Mathematical modeling suggests that the IFN\u2013ADAR\u2013APOL1 network functions as an incoherent feed-forward loop, a biological circuit capable of generating fast, transient responses to stimuli. Glomeruli from human kidney biopsies exhibited widespread editing of APOL1 Alu-dsRNA, while the transgenic mouse model closely replicated the edited sites in humans. APOL1 expression in mice was inversely correlated with Adar1 expression under IFN-\u03b3 stimuli, supporting the idea that ADAR regulates APOL1 levels in\u00a0vivo. ADAR-mediated A-to-I editing is an important regulator of APOL1 expression that could impact both penetrance and severity of APOL1-associated kidney disease.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2210150119","type":"journal-article","created":{"date-parts":[[2022,10,25]],"date-time":"2022-10-25T13:56:17Z","timestamp":1666706177000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":20,"title":["ADAR regulates APOL1 via A-to-I RNA editing by inhibition of MDA5 activation in a paradoxical biological circuit"],"prefix":"10.1073","volume":"119","author":[{"given":"Cristian V.","family":"Riella","sequence":"first","affiliation":[{"name":"Nephrology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215"},{"name":"Department of Medicinie, Harvard Medical School, Boston, MA 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