<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jin J</submitter><funding>Hangzhou Science and Technology Plan Development Project</funding><funding>National Key R&amp;D Program of China</funding><funding>CAMS Innovation Fund for Medical Sciences</funding><funding>Medical and Health Science and Technology Project of Hangzhou</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Research and Development Program of China</funding><pagination>e13493</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10623940</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>56(11)</volume><pubmed_abstract>Cell migration and proliferation are conducive to wound healing; however, regulating cell proliferation remains challenging, and excessive proliferation is an important cause of scar hyperplasia. Here, we aimed to explore how a subvacuum environment promotes wound epithelisation without affecting scar hyperplasia. Human immortalized keratinocyte cells and human skin fibroblasts were cultured under subvacuum conditions (1/10 atmospheric pressure), and changes in cell proliferation and migration, target protein content, calcium influx, and cytoskeleton and membrane fluidity were observed. Mechanical calcium (Ca&lt;sup>2+&lt;/sup> ) channel blockers were used to prevent Ca&lt;sup>2+&lt;/sup> influx for reverse validation. A rat wound model was used to elucidate the mechanism of the subvacuum dressing in </pubmed_abstract><journal>Cell proliferation</journal><pubmed_title>Subvacuum environment-enhanced cell migration promotes wound healing without increasing hypertrophic scars caused by excessive cell proliferation.</pubmed_title><pmcid>PMC10623940</pmcid><funding_grant_id>2019YFA0110603</funding_grant_id><funding_grant_id>2019YFA0110602</funding_grant_id><funding_grant_id>2019YFA0110601</funding_grant_id><funding_grant_id>2019YFA0110600</funding_grant_id><funding_grant_id>B20200432</funding_grant_id><funding_grant_id>81772125</funding_grant_id><funding_grant_id>2019-I2M-5-076</funding_grant_id><funding_grant_id>81930057</funding_grant_id><funding_grant_id>81772076</funding_grant_id><funding_grant_id>20210133X01</funding_grant_id><pubmed_authors>Fang H</pubmed_authors><pubmed_authors>Xia ZF</pubmed_authors><pubmed_authors>Pan BH</pubmed_authors><pubmed_authors>Zhu SH</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Wu GS</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Wang KA</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Zhu LL</pubmed_authors><pubmed_authors>Zhu BH</pubmed_authors><pubmed_authors>Jin J</pubmed_authors><pubmed_authors>Yu SS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Subvacuum environment-enhanced cell migration promotes wound healing without increasing hypertrophic scars caused by excessive cell proliferation.</name><description>Cell migration and proliferation are conducive to wound healing; however, regulating cell proliferation remains challenging, and excessive proliferation is an important cause of scar hyperplasia. Here, we aimed to explore how a subvacuum environment promotes wound epithelisation without affecting scar hyperplasia. Human immortalized keratinocyte cells and human skin fibroblasts were cultured under subvacuum conditions (1/10 atmospheric pressure), and changes in cell proliferation and migration, target protein content, calcium influx, and cytoskeleton and membrane fluidity were observed. Mechanical calcium (Ca&lt;sup>2+&lt;/sup> ) channel blockers were used to prevent Ca&lt;sup>2+&lt;/sup> influx for reverse validation. A rat wound model was used to elucidate the mechanism of the subvacuum dressing in </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2025-04-21T23:54:07.614Z</modification><creation>2025-04-05T19:19:41.005Z</creation></dates><accession>S-EPMC10623940</accession><cross_references><pubmed>37128180</pubmed><doi>10.1111/cpr.13493</doi></cross_references></HashMap>