Qiannan Ma, Ella X. Segal, Miles A. Montegut, Suneeti R. Madhavan, Anna R. Jussila, Claire Reynolds, Rachel H. Wyetzner, Megan Gregory, Elif Ertugral, Chandrasekhar Kothapalli, Radhika P. Atit
{"title":"成熟真皮脂肪细胞中的Wnt激活通过atgl依赖性脂肪分解导致脂肪营养不良和皮肤纤维化","authors":"Qiannan Ma, Ella X. Segal, Miles A. Montegut, Suneeti R. Madhavan, Anna R. Jussila, Claire Reynolds, Rachel H. Wyetzner, Megan Gregory, Elif Ertugral, Chandrasekhar Kothapalli, Radhika P. Atit","doi":"10.1096/fj.202501380R","DOIUrl":null,"url":null,"abstract":"<p>Accumulation of extracellular matrix (ECM) and dermal adipocyte lipodystrophy occurs during skin fibrosis, which compromises the skin's flexibility and function. Sustained Wnt activation in dermal progenitor cells leads to fibrotic ECM thickening in the dermis and lipodystrophy of dermal white adipose tissue (DWAT). Mouse genetic models with lineage tracing demonstrate that Wnt activation in mature dermal adipocytes is sufficient to induce adipocyte lipodystrophy and fibrotic ECM remodeling in the skin. Upon withdrawal of adipocyte-restricted Wnt activation, lipodystrophy and fibrosis are reversed. Mechanistically, Wnt activation stimulates the Adipose Triglyceride Lipase (ATGL)-mediated lipolysis pathway, and lipolysis is an early event in the skin of Systemic Sclerosis patients. <i>Atgl</i> in dermal adipocytes is functionally required for Wnt-induced lipodystrophy in the DWAT and fibrotic remodeling. Collectively, this study demonstrates that Wnt activation in dermal adipocytes promotes lipolysis, suggesting a therapeutic avenue for the treatment of lipodystrophy and skin fibrosis.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 13","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202501380R","citationCount":"0","resultStr":"{\"title\":\"Wnt Activation in Mature Dermal Adipocytes Leads to Lipodystrophy and Skin Fibrosis via ATGL-Dependent Lipolysis\",\"authors\":\"Qiannan Ma, Ella X. Segal, Miles A. Montegut, Suneeti R. Madhavan, Anna R. Jussila, Claire Reynolds, Rachel H. Wyetzner, Megan Gregory, Elif Ertugral, Chandrasekhar Kothapalli, Radhika P. Atit\",\"doi\":\"10.1096/fj.202501380R\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Accumulation of extracellular matrix (ECM) and dermal adipocyte lipodystrophy occurs during skin fibrosis, which compromises the skin's flexibility and function. Sustained Wnt activation in dermal progenitor cells leads to fibrotic ECM thickening in the dermis and lipodystrophy of dermal white adipose tissue (DWAT). Mouse genetic models with lineage tracing demonstrate that Wnt activation in mature dermal adipocytes is sufficient to induce adipocyte lipodystrophy and fibrotic ECM remodeling in the skin. Upon withdrawal of adipocyte-restricted Wnt activation, lipodystrophy and fibrosis are reversed. Mechanistically, Wnt activation stimulates the Adipose Triglyceride Lipase (ATGL)-mediated lipolysis pathway, and lipolysis is an early event in the skin of Systemic Sclerosis patients. <i>Atgl</i> in dermal adipocytes is functionally required for Wnt-induced lipodystrophy in the DWAT and fibrotic remodeling. Collectively, this study demonstrates that Wnt activation in dermal adipocytes promotes lipolysis, suggesting a therapeutic avenue for the treatment of lipodystrophy and skin fibrosis.</p>\",\"PeriodicalId\":50455,\"journal\":{\"name\":\"The FASEB Journal\",\"volume\":\"39 13\",\"pages\":\"\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-07-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202501380R\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The FASEB Journal\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1096/fj.202501380R\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The FASEB Journal","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1096/fj.202501380R","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Wnt Activation in Mature Dermal Adipocytes Leads to Lipodystrophy and Skin Fibrosis via ATGL-Dependent Lipolysis
Accumulation of extracellular matrix (ECM) and dermal adipocyte lipodystrophy occurs during skin fibrosis, which compromises the skin's flexibility and function. Sustained Wnt activation in dermal progenitor cells leads to fibrotic ECM thickening in the dermis and lipodystrophy of dermal white adipose tissue (DWAT). Mouse genetic models with lineage tracing demonstrate that Wnt activation in mature dermal adipocytes is sufficient to induce adipocyte lipodystrophy and fibrotic ECM remodeling in the skin. Upon withdrawal of adipocyte-restricted Wnt activation, lipodystrophy and fibrosis are reversed. Mechanistically, Wnt activation stimulates the Adipose Triglyceride Lipase (ATGL)-mediated lipolysis pathway, and lipolysis is an early event in the skin of Systemic Sclerosis patients. Atgl in dermal adipocytes is functionally required for Wnt-induced lipodystrophy in the DWAT and fibrotic remodeling. Collectively, this study demonstrates that Wnt activation in dermal adipocytes promotes lipolysis, suggesting a therapeutic avenue for the treatment of lipodystrophy and skin fibrosis.
期刊介绍:
The FASEB Journal publishes international, transdisciplinary research covering all fields of biology at every level of organization: atomic, molecular, cell, tissue, organ, organismic and population. While the journal strives to include research that cuts across the biological sciences, it also considers submissions that lie within one field, but may have implications for other fields as well. The journal seeks to publish basic and translational research, but also welcomes reports of pre-clinical and early clinical research. In addition to research, review, and hypothesis submissions, The FASEB Journal also seeks perspectives, commentaries, book reviews, and similar content related to the life sciences in its Up Front section.