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Different experimental rodent models have been established for simulating NS, however, not all of them feature sodium retention which requires proteinuria to exceed a certain threshold. In rats, puromycin aminonucleoside nephrosis (PAN) is a classic NS model introduced in 1955 that was adopted as doxorubicin\u2010induced nephropathy (DIN) in 129S1\/SvImJ mice. In recent years, mice with inducible podocin deletion (<jats:italic>Nphs2<\/jats:italic><jats:sup><jats:italic>\u0394ipod<\/jats:italic><\/jats:sup>) or podocyte apoptosis (POD\u2010ATTAC) have been developed. In these models, sodium retention is thought to be caused by activation of the epithelial sodium channel (ENaC) in the distal nephron through aberrantly filtered serine proteases or proteasuria. Strikingly, rodent NS models follow an identical chronological time course after the development of proteinuria featuring sodium retention within days and spontaneous reversal thereafter. In DIN and<jats:italic>Nphs2<\/jats:italic><jats:sup><jats:italic>\u0394ipod<\/jats:italic><\/jats:sup>mice, inhibition of ENaC by amiloride or urinary serine protease activity by aprotinin prevents sodium retention, opening up new and promising therapeutic approaches that could be translated into the treatment of nephrotic patients. However, the essential serine protease(s) responsible for ENaC activation is (are) still unknown. With the use of nephrotic rodent models, there is the possibility that this (these) will be identified in the future. This review summarizes the various rodent models used to study experimental nephrotic syndrome and the insights gained from these models with regard to the pathophysiology of sodium retention.<\/jats:p>","DOI":"10.1111\/apha.13844","type":"journal-article","created":{"date-parts":[[2022,5,15]],"date-time":"2022-05-15T07:59:51Z","timestamp":1652601591000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Rodent models to study sodium retention in experimental nephrotic syndrome"],"prefix":"10.1111","volume":"235","author":[{"given":"Mengyun","family":"Xiao","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Diabetology and Nephrology, Department of Internal Medicine University Hospital T\u00fcbingen T\u00fcbingen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0169-3948","authenticated-orcid":false,"given":"Bernhard N.","family":"Bohnert","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetology and Nephrology, Department of Internal Medicine University Hospital T\u00fcbingen T\u00fcbingen Germany"},{"name":"Institute of Diabetes Research and Metabolic Diseases (IDM) of the Helmholtz Center Munich at the University T\u00fcbingen T\u00fcbingen Germany"},{"name":"German Center for Diabetes Research (DZD) at the University T\u00fcbingen T\u00fcbingen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Florian","family":"Grahammer","sequence":"additional","affiliation":[{"name":"III. 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