<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang Y</submitter><funding>The 111 Project</funding><funding>The National Natural Science Foundation of China</funding><pagination>8444</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11897129</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Skin fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) in the dermis, can lead to hypertrophic scars and impaired mobility. The ErbB family of receptor tyrosine kinases, including ErbB1 and ErbB2, plays a crucial role in organ fibrosis, but their specific impact on skin fibrosis is less understood. This study investigated the role of ErbB1 and ErbB2 in skin fibrosis and the therapeutic potential of lapatinib, a dual ErbB1 and ErbB2 tyrosine kinase inhibitor. Using qPCR, cell culture assays, Western blotting, and in vivo models, we found significant upregulation of ErbB1 and ErbB2 in keloid tissues and fibroblasts. Lapatinib treatment resulted in a dose-dependent decrease in ErbB1 and ErbB2 expression, which suppressed the expression of fibroblast activation ma</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Lapatinib ameliorates skin fibrosis by inhibiting TGF-β1/Smad and non-Smad signaling pathway.</pubmed_title><pmcid>PMC11897129</pmcid><funding_grant_id>B20016</funding_grant_id><funding_grant_id>82370073</funding_grant_id><pubmed_authors>Zhang T</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Song H</pubmed_authors><pubmed_authors>Yang C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lapatinib ameliorates skin fibrosis by inhibiting TGF-β1/Smad and non-Smad signaling pathway.</name><description>Skin fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) in the dermis, can lead to hypertrophic scars and impaired mobility. The ErbB family of receptor tyrosine kinases, including ErbB1 and ErbB2, plays a crucial role in organ fibrosis, but their specific impact on skin fibrosis is less understood. This study investigated the role of ErbB1 and ErbB2 in skin fibrosis and the therapeutic potential of lapatinib, a dual ErbB1 and ErbB2 tyrosine kinase inhibitor. Using qPCR, cell culture assays, Western blotting, and in vivo models, we found significant upregulation of ErbB1 and ErbB2 in keloid tissues and fibroblasts. Lapatinib treatment resulted in a dose-dependent decrease in ErbB1 and ErbB2 expression, which suppressed the expression of fibroblast activation ma</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2025-04-04T01:28:54.543Z</modification><creation>2025-04-04T01:28:54.543Z</creation></dates><accession>S-EPMC11897129</accession><cross_references><pubmed>40069312</pubmed><doi>10.1038/s41598-025-92687-1</doi></cross_references></HashMap>