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The current CPN mechanism of action for tumorigenesis is largely based on its associated increase in tubular cell proliferation without regard to preceding subcellular degenerative changes. Combing through the published literature from multiple biology disciplines provided insight into the preceding cellular events. Mechanistic pathways involved in the progressive age-related decline in rodent kidney function and several key inflexion points have been identified. These critical pathway factors were then connected using data from renal models from multiple rodent strains, other species, and mechanistic work in humans to form a cohesive picture of pathways and protein interactions. Abundant data linked similar renal pathologies to local events involving hypoxia (hypoxia-inducible factor 1\u03b1), altered intrarenal renin\u2013angiotensin system (RAS), oxidative stress (nitric oxide), and pro-inflammatory pathways (transforming growth factor \u03b2), with positive feedback loops and downstream effectors amplifying the injury and promoting scarring. Intrarenal RAS alterations seem to be central to all these events and may be critical to CPN development and progression.<\/jats:p>","DOI":"10.1177\/0192623319861367","type":"journal-article","created":{"date-parts":[[2019,7,8]],"date-time":"2019-07-08T00:46:28Z","timestamp":1562546788000},"page":"799-816","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":13,"title":["Intrarenal Renin\u2013Angiotensin System Involvement in the Pathogenesis of Chronic Progressive Nephropathy\u2014Bridging the Informational Gap Between Disciplines"],"prefix":"10.1177","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9788-2908","authenticated-orcid":false,"given":"Leslie A.","family":"Obert","sequence":"first","affiliation":[{"name":"GlaxoSmithKline, Collegeville, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4608-5543","authenticated-orcid":false,"given":"Kendall 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