{"title":"Fibroblastos sinoviales","authors":"Elena Izquierdo , José Luis Pablos","doi":"10.1016/j.semreu.2013.06.001","DOIUrl":null,"url":null,"abstract":"<div><p>Synovial fibroblasts (SF) or fibroblast-like synoviocytes are the major resident cellular component of joint synovial membrane. Numerous studies support the hypothesis that SF play an important role in the pathogenesis of rheumatoid arthritis (RA). In the RA synovial membrane, SF increase in number (hyperplasia) and exhibit an altered phenotype that persists in culture in the absence of external stimuli. These abnormalities are associated with the activation of specific signalling pathways that promote cell growth and the expression of multiple factors such as cytokines, chemokines, growth factors, adhesion molecules, and matrix degradation enzymes. The activation and expansion of SF appear to contribute to the recruitment, retention and activation of inflammatory cells, new blood vessel formation (angiogenesis), and bone and cartilage destruction. The relative contribution of SF to these processes is very important in animal models but has not been determined in human RA due to the lack of treatment interventions specifically targeting these cells. The identification of the molecular pathways involved in the altered phenotype of rheumatoid SF and their pathophysiological contribution are the basis for the development of new therapeutic alternatives for chronic inflammation and joint damage not targeting the immune system.</p></div>","PeriodicalId":101152,"journal":{"name":"Seminarios de la Fundación Espa?ola de Reumatología","volume":"14 4","pages":"Pages 121-128"},"PeriodicalIF":0.0000,"publicationDate":"2013-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.semreu.2013.06.001","citationCount":"1","resultStr":"{\"title\":\"Fibroblastos sinoviales\",\"authors\":\"Elena Izquierdo , José Luis Pablos\",\"doi\":\"10.1016/j.semreu.2013.06.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Synovial fibroblasts (SF) or fibroblast-like synoviocytes are the major resident cellular component of joint synovial membrane. Numerous studies support the hypothesis that SF play an important role in the pathogenesis of rheumatoid arthritis (RA). In the RA synovial membrane, SF increase in number (hyperplasia) and exhibit an altered phenotype that persists in culture in the absence of external stimuli. These abnormalities are associated with the activation of specific signalling pathways that promote cell growth and the expression of multiple factors such as cytokines, chemokines, growth factors, adhesion molecules, and matrix degradation enzymes. The activation and expansion of SF appear to contribute to the recruitment, retention and activation of inflammatory cells, new blood vessel formation (angiogenesis), and bone and cartilage destruction. The relative contribution of SF to these processes is very important in animal models but has not been determined in human RA due to the lack of treatment interventions specifically targeting these cells. The identification of the molecular pathways involved in the altered phenotype of rheumatoid SF and their pathophysiological contribution are the basis for the development of new therapeutic alternatives for chronic inflammation and joint damage not targeting the immune system.</p></div>\",\"PeriodicalId\":101152,\"journal\":{\"name\":\"Seminarios de la Fundación Espa?ola de Reumatología\",\"volume\":\"14 4\",\"pages\":\"Pages 121-128\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2013-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.semreu.2013.06.001\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Seminarios de la Fundación Espa?ola de Reumatología\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1577356613000419\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Seminarios de la Fundación Espa?ola de Reumatología","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1577356613000419","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Synovial fibroblasts (SF) or fibroblast-like synoviocytes are the major resident cellular component of joint synovial membrane. Numerous studies support the hypothesis that SF play an important role in the pathogenesis of rheumatoid arthritis (RA). In the RA synovial membrane, SF increase in number (hyperplasia) and exhibit an altered phenotype that persists in culture in the absence of external stimuli. These abnormalities are associated with the activation of specific signalling pathways that promote cell growth and the expression of multiple factors such as cytokines, chemokines, growth factors, adhesion molecules, and matrix degradation enzymes. The activation and expansion of SF appear to contribute to the recruitment, retention and activation of inflammatory cells, new blood vessel formation (angiogenesis), and bone and cartilage destruction. The relative contribution of SF to these processes is very important in animal models but has not been determined in human RA due to the lack of treatment interventions specifically targeting these cells. The identification of the molecular pathways involved in the altered phenotype of rheumatoid SF and their pathophysiological contribution are the basis for the development of new therapeutic alternatives for chronic inflammation and joint damage not targeting the immune system.