{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T19:53:06Z","timestamp":1784231586398,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,12,6]],"date-time":"2017-12-06T00:00:00Z","timestamp":1512518400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81272121"],"award-info":[{"award-number":["81272121"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2018,1]]},"abstract":"Abstract<\/jats:title>A hypertrophic scar (HS<\/jats:styled-content>) is caused by abnormal proliferation of dermal fibroblasts. Thus, promoting hypertrophic scar fibroblast (HSFB<\/jats:styled-content>) apoptosis is an effective strategy for HS<\/jats:styled-content> therapy. Ursolic acid (UA<\/jats:styled-content>) has been widely used as an inducer of apoptosis in diverse cancers. However, whether UA<\/jats:styled-content> plays an inhibitory role in HS<\/jats:styled-content> formation is still unknown. In our study, UA<\/jats:styled-content> was used to treat HSFB<\/jats:styled-content>s and the cell viability, apoptosis, and collagen synthesis were determined by a Cell Counting Kit 8 assay, flow cytometry, and an H3<\/jats:sup>\u2010proline incorporation assay, respectively. Autophagy activity was detected by LC<\/jats:styled-content>3 immunoblotting and electron microscopy, and siRNA<\/jats:styled-content>s targeting Beclin\u20101 were used to inhibit autophagy. Western blotting was performed to investigate the molecular changes in HSFB<\/jats:styled-content>s after various treatments. We found that UA<\/jats:styled-content> inhibited collagen synthesis and induced cell apoptosis in HSFB<\/jats:styled-content>s, evidenced by the deregulated expression of Bim, Bcl\u20102 and Cyto C. Furthermore, we demonstrated that UA<\/jats:styled-content> induced autophagy and inactivation of autophagy promoted UA<\/jats:styled-content>\u2010induced apoptosis and collagen synthesis inhibition in HSFB<\/jats:styled-content>s. Molecular investigation indicated that UA<\/jats:styled-content>\u2010induced autophagy through upregulation of Beclin\u20101 and knockdown of Beclin\u20101 prevent UA<\/jats:styled-content>\u2010induced autophagy. Overexpression of Bcl\u20102 prevents UA<\/jats:styled-content>\u2010induced autophagy, Beclin\u20101 upregulation, apoptosis and collagen synthesis inhibition in HSFB<\/jats:styled-content>s. Collectively, our study demonstrated that UA<\/jats:styled-content> is a novel agent for inhibiting HS<\/jats:styled-content> formation by promoting apoptosis, especially in combination with an autophagy inhibitor. Our results provide strong evidence of the application of UA<\/jats:styled-content> in clinical HS<\/jats:styled-content> treatment.<\/jats:p>","DOI":"10.1111\/exd.13410","type":"journal-article","created":{"date-parts":[[2017,8,2]],"date-time":"2017-08-02T14:52:37Z","timestamp":1501685557000},"page":"58-63","source":"Crossref","is-referenced-by-count":32,"title":["Inactivation of Beclin\u20101\u2010dependent autophagy promotes ursolic acid\u2010induced apoptosis in hypertrophic scar fibroblasts"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1911-2315","authenticated-orcid":false,"given":"Chuan","family":"Cao","sequence":"first","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenping","family":"Wang","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lele","family":"Lu","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Wang","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"XiaoSong","family":"Chen","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Concord Hospital of the Fujian Medical University Fuzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Guo","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shirong","family":"Li","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junzi","family":"Jiang","sequence":"additional","affiliation":[{"name":"Plastic Surgery Department of Southwest Hospital Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,12,6]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/ejs.6161681002"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.3892\/ijmm.2015.2299"},{"key":"e_1_2_8_4_1","doi-asserted-by":"crossref","first-page":"271","DOI":"10.1016\/S0749-0712(21)00203-1","volume":"16","author":"Scott P. 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