{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:41:02Z","timestamp":1791380462882,"version":"4.3.3"},"reference-count":153,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T00:00:00Z","timestamp":1366329600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Interstitial infiltrates, consisting of macrophages and other inflammatory cells, have been consistently reported in human and animal models of polycystic kidney diseases (\n                    <jats:styled-content style=\"fixed-case\">PKD<\/jats:styled-content>\n                    ). However, the mechanisms underlying this inflammation are not well defined. Evidence suggests that interstitial inflammation in\n                    <jats:styled-content style=\"fixed-case\">PKD<\/jats:styled-content>\n                    is driven by pro\u2010inflammatory chemoattractants such as monocyte chemoattractant protein\u20101 (\n                    <jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\n                    \u20101), and cytokines such as tumour necrosis factor (\n                    <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\n                    )\u2010\u03b1. Putative upregulated inflammatory pathways include\n                    <jats:styled-content style=\"fixed-case\">JAK\u2010STAT<\/jats:styled-content>\n                    and nuclear factor (\n                    <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\n                    )\u2010\u03ba\n                    <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\n                    signalling. In addition, the genetic mutations of\n                    <jats:styled-content style=\"fixed-case\">PKD<\/jats:styled-content>\n                    may further complicate the relationship between inflammation and cystic disease, by increasing the susceptibility to inflammatory injury, and facilitating interactions between the genetically determined cystoproteins and biological mediators of inflammation. Moreover, the roles of interstitial inflammation in promoting cyst growth and progression to kidney failure in\n                    <jats:styled-content style=\"fixed-case\">PKD<\/jats:styled-content>\n                    are not clearly understood. Although anti\u2010inflammatory therapies have attenuated cystogenesis in animal models, inflammatory cells may also have reparative actions. Thus, in developing therapies for\n                    <jats:styled-content style=\"fixed-case\">PKD<\/jats:styled-content>\n                    , it is prudent to consider the potential negative outcomes of ablating inflammation, and whether it is more viable to target certain inflammatory pathways over others.\n                  <\/jats:p>","DOI":"10.1111\/nep.12045","type":"journal-article","created":{"date-parts":[[2013,3,1]],"date-time":"2013-03-01T13:54:15Z","timestamp":1362146055000},"page":"317-330","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["Role of interstitial inflammation in the pathogenesis of polycystic kidney disease"],"prefix":"10.1111","volume":"18","author":[{"given":"Michelle HT","family":"Ta","sequence":"first","affiliation":[{"name":"Centre for Transplant and Renal Research Westmead Millennium Institute The University of Sydney  Sydney New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David CH","family":"Harris","sequence":"additional","affiliation":[{"name":"Centre for Transplant and Renal Research Westmead Millennium Institute The University of Sydney  Sydney New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gopala K","family":"Rangan","sequence":"additional","affiliation":[{"name":"Centre for Transplant and Renal Research Westmead Millennium Institute The University of Sydney  Sydney New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,4,19]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.60.101707.125712"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng0695-151"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1339"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng833"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.39.020188.001153"},{"key":"e_1_2_11_7_1","doi-asserted-by":"crossref","first-page":"257","DOI":"10.1136\/jmg.8.3.257","article-title":"Polycystic disease of kidney and liver presenting in childhood","volume":"8","author":"Blyth H","year":"1971","journal-title":"J. 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