{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T19:30:36Z","timestamp":1785526236230,"version":"3.56.0"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Vascular calcification is frequent among patients with chronic kidney disease, in which vascular smooth muscle cells (VSMCs) play a key pathological role. Our previous research revealed that the E3 ubiquitin ligase RNF10 (ring finger protein 10) regulates VSMC hyperproliferation and apoptosis; however, the function of RNF10 in vascular calcification remains unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Serum RNF10 levels were assessed in 2 independent cross-sectional chronic kidney disease patient cohorts with vascular calcification. RNF10 expression was assessed in calcified rat aortas and VSMCs. The effects of RNF10 on vascular calcification were evaluated in\n                      <jats:italic toggle=\"yes\">RNF10<\/jats:italic>\n                      knock-in rats and RNF10 overexpressed VSMCs. To investigate the underlying mechanism, RNA-seq (RNA sequencing), ChIP-seq (chromatin immunoprecipitation sequencing), ChIP-qPCR (chromatin immunoprecipitation quantitative PCR), and luciferase reporter assays were performed. Gain- and loss-of-function experiments targeting Rbpjk (recombination signal binding protein for immunoglobulin kappa J region) were conducted in vivo and in vitro.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Circulating RNF10 levels were significantly reduced in chronic kidney disease patients with vascular calcification, and RNF10 protein expression was reduced in calcified rat aortas and VSMCs.\n                      <jats:italic toggle=\"yes\">RNF10<\/jats:italic>\n                      knock-in alleviated vascular calcification without obvious adverse effects on other major organs. In vitro, RNF10 overexpression attenuated calcification and reduced the expression of osteogenic markers. Notably, pharmacological inhibition of the ubiquitin-proteasome system did not impair RNF10\u2019s anticalcific activity. Nuclear RNF10 expression was increased in calcified VSMCs, supporting a noncanonical and transcriptional regulatory role. Integrated analyses identified that RNF10 negatively regulated\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      expression during vascular calcification, rather than acting through the ubiquitin-proteasome system. Moreover, viral\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      overexpression partially reversed the protective effects of RNF10 in vivo and in vitro and increased osteogenic marker expression, whereas siRNA-mediated\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      knockdown reduced the marker expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      RNF10 depletion serves as the initiating factor that triggers\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      -driven osteogenic differentiation during chronic kidney disease\u2013associated vascular calcification. The protective role of RNF10 involves\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      negative expression regulation rather than E3 ubiquitin ligase activity. This RNF10-\n                      <jats:italic toggle=\"yes\">Rbpjk<\/jats:italic>\n                      regulatory axis provides a new perspective for developing prevention and treatment strategies for vascular calcification.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.324395","type":"journal-article","created":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T09:00:21Z","timestamp":1776330021000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["E3 Ubiquitin Ligase RNF10 Negatively Regulates Rbpjk Expression During Vascular Calcification in Chronic Kidney Disease"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0607-2043","authenticated-orcid":true,"given":"Guiquan","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingyang","family":"Ran","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9356-159X","authenticated-orcid":true,"given":"Shuqin","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingsong","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0555-8372","authenticated-orcid":true,"given":"Pengfei","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4453-8956","authenticated-orcid":true,"given":"Chunxia","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, 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