{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T11:03:21Z","timestamp":1789988601557,"version":"4.0.1"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,1,29]],"date-time":"2025-01-29T00:00:00Z","timestamp":1738108800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,1,29]],"date-time":"2025-01-29T00:00:00Z","timestamp":1738108800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>The goal of this study was to explore new candidate genes and pathogenesis mechanisms of nonsyndromic hereditary gingival fibromatosis (nsHGF) and to provide an experimental basis for the diagnosis of nsHGF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Whole\u2010exome sequencing (WES) was performed on peripheral blood DNA from three nsHGF family members to screen for new candidate genes, and Sanger sequencing and related databases were used to verify the pathogenicity of this gene deficiency. Moreover, the effects of gene deficiency on the biological characteristics of human gingival fibroblasts (HGFs) were evaluated via cell proliferation assays, extracellular matrix (ECM) deposition detection, cell apoptosis and cell cycle assessment, cell migration and gene expression analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A novel missense mutation in\n                      <jats:italic>dual\u2010specificity phosphatase 8<\/jats:italic>\n                      (\n                      <jats:italic>DUSP8<\/jats:italic>\n                      , c.1348C&gt;T, p.R450C), which is in the nsHGF\u2010related GINGF4 locus, was identified via WES analysis. A functional study revealed that knocking down DUSP8 expression increased cell proliferation, cell migration and the expression of profibrotic factors (particularly\n                      <jats:italic>COL1A1<\/jats:italic>\n                      ), inhibited cell apoptosis, and ultimately resulted in nsHGF. Similarly, this\n                      <jats:italic>DUSP8<\/jats:italic>\n                      mutation inhibited the expression of the encoded protein and promoted cell proliferation and the expression of profibrotic factors. In addition, both\n                      <jats:italic>DUSP8<\/jats:italic>\n                      knockdown and\n                      <jats:italic>DUSP8<\/jats:italic>\n                      mutation induced nsHGF by accelerating glycolysis and panlysine lactylation (Kla) to promote cell proliferation and the expression of ECM\u2010related factors.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>DUSP8<\/jats:italic>\n                      deficiency might be a novel pathogenic factor that contributes to nsHGF.\n                    <\/jats:p>\n                  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