{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T10:34:51Z","timestamp":1776940491557,"version":"3.51.4"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2022,1,10]],"date-time":"2022-01-10T00:00:00Z","timestamp":1641772800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"Zhejiang Provincial Natural Science Foundation of China","award":["LQ21H030011"],"award-info":[{"award-number":["LQ21H030011"]}]},{"name":"Zhejiang Provincial Natural Science Foundation of China","award":["LY20H030005"],"award-info":[{"award-number":["LY20H030005"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770547"],"award-info":[{"award-number":["81770547"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,6,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Intestinal fibrosis is a common complication of Crohn\u2019s disease (CD) and is characterized by the excessive accumulation of extracellular matrix produced by activated myofibroblasts. Caveolin-1 (CAV1) inhibits fibrosis. However, limited data show that CAV1 affects intestinal fibrosis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Human CD tissue samples were gained from patients with CD who underwent surgical resection of the intestine and were defined as stenotic or nonstenotic areas. A dextran sodium sulfate\u2013induced mouse model of intestinal fibrosis was established. For in vitro experiments, we purchased CCD-18Co intestinal fibrosis cells and isolated and cultured human primary colonic fibroblasts. These fibroblasts were activated by transforming growth factor \u03b2 administration for 48 hours. In the functional experiments, a specific small interfering RNA or overexpression plasmid was transfected into fibroblasts. The messenger RNA levels of fibrosis markers, such as \u03b1-smooth muscle actin, fibronectin, connective tissue growth factor, and collagen I1\u03b1, were determined using quantitative polymerase chain reaction. Western blot analysis was applied to detect the expression of CAV1, SQSTM1\/p62 (sequestosome 1), and other fibrosis markers.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>In human CD samples and the dextran sodium sulfate\u2013induced mouse model of intestinal fibrosis, we observed a downregulation of CAV1 in fibrosis-activated areas. Mechanistically, CAV1 knockdown in both human primary colonic fibroblasts and CCD-18Co cells promoted fibroblast activation, while CAV1 overexpression inhibited fibroblast activation in vitro. We found that SQSTM1\/p62 positively correlated with CAV1 expression levels in patients with CD and that it was indirectly modulated by CAV1 expression. Rescue experiments showed that CAV1 decreased primary human intestinal fibroblast activation by inhibiting fibroblast autophagy through the modulation of SQSTM1\/p62.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Our data demonstrate that CAV1 deficiency induces fibroblast activation by indirectly regulating SQSTM1\/p62 to promote fibroblast autophagy. CAV1 or SQSTM1\/p62 may be potential therapeutic targets for intestinal fibrosis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ibd\/izab342","type":"journal-article","created":{"date-parts":[[2022,1,12]],"date-time":"2022-01-12T18:57:10Z","timestamp":1642013830000},"page":"923-935","source":"Crossref","is-referenced-by-count":23,"title":["Caveolin-1 Alleviates Crohn\u2019s Disease\u2013induced Intestinal Fibrosis by Inhibiting Fibroblasts Autophagy Through Modulating Sequestosome 1"],"prefix":"10.1093","volume":"28","author":[{"given":"Mengli","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, First Affiliated Hospital, College of Medicine, Zhejiang University , Hangzhou , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, First Affiliated Hospital, College of Medicine, Zhejiang University , Hangzhou , 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