{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T15:50:16Z","timestamp":1753890616480,"version":"3.41.2"},"reference-count":49,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T00:00:00Z","timestamp":1708992000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Cell division cycle 42 (CDC42) regulates CD4<jats:sup>+<\/jats:sup><jats:italic>T<\/jats:italic>-cell differentiation and participates in vascular stiffness and atherosclerosis and is involved in the progression of Stanford type B aortic dissection (TBAD). This study aimed to explore the correlation between serum CDC42 level and CD4<jats:sup>+<\/jats:sup><jats:italic>T<\/jats:italic> cell subsets and in-hospital mortality in TBAD patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Serum CDC42 and peripheral blood T-helper (Th) 1, Th2, and Th17 cells were detected in 127 TBAD patients by enzyme-linked immunosorbent assay and flow cytometry, respectively. Serum CDC42 was also quantified in 30 healthy controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Serum CDC42 was decreased in TBAD patients vs. healthy controls (median [interquartile range (IQR)]: 418.0 (228.0\u2013761.0)\u2005pg\/ml vs. 992.0 (716.3\u20131,445.8)\u2005pg\/ml, <jats:italic>P\u2009<\/jats:italic>&amp;lt;\u20090.001). In TBAD patients, serum CDC42 was negatively correlated with Th17 cells (<jats:italic>P\u2009<\/jats:italic>=\u20090.001), but not Th1 (<jats:italic>P\u2009<\/jats:italic>=\u20090.130) or Th2 cells (<jats:italic>P\u2009<\/jats:italic>=\u20090.098). Seven (5.5%) patients experienced in-hospital mortality. Serum CDC42 was reduced in patients who experienced in-hospital mortality vs. those who did not (median (IQR): 191.0 (145.0\u2013345.0)\u2005pg\/ml vs. 451.5 (298.3\u2013766.8)\u2005pg\/ml, <jats:italic>P\u2009<\/jats:italic>=\u20090.006). By receiver operating characteristic analysis, serum CDC42 showed a good ability for estimating in-hospital mortality [area under curve\u2009=\u20090.809, 95% confidence interval (CI)\u2009=\u20090.662\u20130.956]. By the multivariate logistic regression analysis, elevated serum CDC42 [odd ratio (OR)\u2009=\u20090.994, 95% CI\u2009=\u20090.998\u20131.000, <jats:italic>P\u2009<\/jats:italic>=\u20090.043] was independently correlated with lower risk of in-hospital mortality, while higher age (OR\u2009=\u20091.157, 95% CI\u2009=\u20091.017\u20131.316, <jats:italic>P\u2009<\/jats:italic>=\u20090.027) was an independent factor for increased risk of in-hospital mortality.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Serum CDC42 negatively associates with Th17 cells and is independently correlated with decreased in-hospital mortality risk in TBAD patients.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fcvm.2024.1324345","type":"journal-article","created":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T04:37:13Z","timestamp":1709008633000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Correlation of the 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