{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:33:10Z","timestamp":1792787590183,"version":"4.5.0"},"reference-count":44,"publisher":"American Society for Clinical Investigation","issue":"9","funder":[{"DOI":"10.13039\/501100001677","name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale","doi-asserted-by":"crossref","award":["Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale"],"award-info":[{"award-number":["Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale"]}],"id":[{"id":"10.13039\/501100001677","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100005413","name":"Universit\u00e9 Paris Descartes","doi-asserted-by":"crossref","award":["Universit\u00e9 Paris Descartes"],"award-info":[{"award-number":["Universit\u00e9 Paris Descartes"]}],"id":[{"id":"10.13039\/501100005413","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002738","name":"Assistance Publique H\u00f4pitaux de Paris","doi-asserted-by":"crossref","award":["Assistance Publique H\u00f4pitaux de Paris"],"award-info":[{"award-number":["Assistance Publique H\u00f4pitaux de Paris"]}],"id":[{"id":"10.13039\/501100002738","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Agence Nationale Recherche","award":["SIGNA-KID"],"award-info":[{"award-number":["SIGNA-KID"]}]},{"name":"Whoami Laboratoire d\u2019Excellence","award":["Whoami Laboratoire d\u2019Excellence"],"award-info":[{"award-number":["Whoami Laboratoire d\u2019Excellence"]}]},{"name":"Pharma Research and Early Development Roche Laboratories","award":["Pharma Research"],"award-info":[{"award-number":["Pharma Research"]}]},{"name":"Pharma Research and Early Development Roche Laboratories","award":["Early Development Roche Laboratories"],"award-info":[{"award-number":["Early Development Roche Laboratories"]}]},{"name":"Institut Roche de Recherche et M\u00e9decine Translationnelle","award":["Institut Roche de Recherche et M\u00e9decine Translationnelle"],"award-info":[{"award-number":["Institut Roche de Recherche et M\u00e9decine Translationnelle"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,5,7]]},"abstract":"<jats:p>\n                    The loss of functional nephrons after kidney injury triggers the compensatory growth of the remaining ones to allow functional adaptation. However, in some cases, these compensatory events activate signaling pathways that lead to pathological alterations and chronic kidney disease. Little is known about the identity of these pathways and how they lead to the development of renal lesions. Here, we combined mouse strains that differently react to nephron reduction with molecular and temporal genome-wide transcriptome studies to elucidate the molecular mechanisms involved in these events. We demonstrated that nephron reduction led to 2 waves of cell proliferation: the first one occurred during the compensatory growth regardless of the genetic background, whereas the second one occurr\ufeffed, after a quiescent phase, exclusively in the sensitive strain and accompanied the development of renal lesions. Similarly, clustering by coinertia analysis revealed the existence of 2 waves of gene expression. Interestingly, we identified type I interferon (IFN) response as an early (first-wave) and specific signature of the sensitive (FVB\/N) mice. Activation of type I IFN response was associated with G\n                    <jats:sub>1<\/jats:sub>\n                    \/S cell cycle arrest, which correlated with p21 nuclear translocation. Remarkably, the transient induction of type I IFN response by poly(I:C) injections during the compensatory growth resulted in renal lesions in otherwise-resistant C57BL6 mice. Collectively, these results suggest that the early molecular and cellular events occurring after nephron reduction determine the risk of developing late renal lesions and point to type I IFN response as a crucial event of the deterioration process.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.126183","type":"journal-article","created":{"date-parts":[[2020,5,6]],"date-time":"2020-05-06T11:01:37Z","timestamp":1588762897000},"source":"Crossref","is-referenced-by-count":21,"title":["Signaling pathways predisposing to chronic kidney disease progression"],"prefix":"10.1172","volume":"5","author":[{"given":"Mohamad","family":"Zaidan","sequence":"first","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale (INSERM), U1151, CNRS UMR 8253, Institut Necker Enfants Malades (INEM), Department of Growth and Signaling, Universit\u00e9 de Paris, Paris, France."},{"name":"Service de N\u00e9phrologie-Transplantation, H\u00f4pital Bic\u00eatre, Assistance Publique \u2013 H\u00f4pitaux de Paris (AP-HP), Le Kremlin-Bic\u00eatre, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martine","family":"Burtin","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale (INSERM), U1151, CNRS UMR 8253, Institut Necker Enfants Malades (INEM), Department of Growth and Signaling, Universit\u00e9 de Paris, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3085-0909","authenticated-orcid":true,"given":"Jitao David","family":"Zhang","sequence":"additional","affiliation":[{"name":"Pharmaceutical Sciences, Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel, Basel, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Blanc","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche 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