The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease
Inflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn’s disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsi...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-09-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/19/10439 |
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| author | Valentina Garlatti Sara Lovisa Silvio Danese Stefania Vetrano |
| author_facet | Valentina Garlatti Sara Lovisa Silvio Danese Stefania Vetrano |
| author_sort | Valentina Garlatti |
| collection | DOAJ |
| description | Inflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn’s disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsible for the progressive narrowing and closure of the intestine, defined as stenosis. Although fibrosis is usually considered the product of chronic inflammation, the substantial failure of anti-inflammatory therapies to target and reduce fibrosis in IBD suggests that fibrosis might be sustained in an inflammation-independent manner. Pharmacological therapies targeting integrins have recently shown great promise in the treatment of IBD. The efficacy of these therapies mainly relies on their capacity to target the integrin-mediated recruitment and functionality of the immune cells at the damage site. However, by nature, integrins also act as mechanosensitive molecules involved in the intracellular transduction of signals and modifications originating from the extracellular matrix. Therefore, understanding integrin signaling in the context of IBD may offer important insights into mechanisms of matrix remodeling, which are uncoupled from inflammation and could underlie the onset and persistency of intestinal fibrosis. In this review, we present the currently available knowledge on the role of integrins in the etiopathogenesis of IBD, highlighting their role in the context of immune-dependent and independent mechanisms. |
| first_indexed | 2024-03-10T07:00:07Z |
| format | Article |
| id | doaj.art-acfc5a3a1eed4044a03bb51cd1ec58b2 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T07:00:07Z |
| publishDate | 2021-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-acfc5a3a1eed4044a03bb51cd1ec58b22023-11-22T16:09:37ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-09-0122191043910.3390/ijms221910439The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel DiseaseValentina Garlatti0Sara Lovisa1Silvio Danese2Stefania Vetrano3IRCCS Humanitas Research Hospital, Rozzano, 20089 Milan, ItalyIRCCS Humanitas Research Hospital, Rozzano, 20089 Milan, ItalyIRCCS Humanitas Research Hospital, Rozzano, 20089 Milan, ItalyIRCCS Humanitas Research Hospital, Rozzano, 20089 Milan, ItalyInflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn’s disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsible for the progressive narrowing and closure of the intestine, defined as stenosis. Although fibrosis is usually considered the product of chronic inflammation, the substantial failure of anti-inflammatory therapies to target and reduce fibrosis in IBD suggests that fibrosis might be sustained in an inflammation-independent manner. Pharmacological therapies targeting integrins have recently shown great promise in the treatment of IBD. The efficacy of these therapies mainly relies on their capacity to target the integrin-mediated recruitment and functionality of the immune cells at the damage site. However, by nature, integrins also act as mechanosensitive molecules involved in the intracellular transduction of signals and modifications originating from the extracellular matrix. Therefore, understanding integrin signaling in the context of IBD may offer important insights into mechanisms of matrix remodeling, which are uncoupled from inflammation and could underlie the onset and persistency of intestinal fibrosis. In this review, we present the currently available knowledge on the role of integrins in the etiopathogenesis of IBD, highlighting their role in the context of immune-dependent and independent mechanisms.https://www.mdpi.com/1422-0067/22/19/10439integrininflammatory bowel diseaseIBDintestinal fibrosisinflammation |
| spellingShingle | Valentina Garlatti Sara Lovisa Silvio Danese Stefania Vetrano The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease International Journal of Molecular Sciences integrin inflammatory bowel disease IBD intestinal fibrosis inflammation |
| title | The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease |
| title_full | The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease |
| title_fullStr | The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease |
| title_full_unstemmed | The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease |
| title_short | The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease |
| title_sort | multiple faces of integrin ecm interactions in inflammatory bowel disease |
| topic | integrin inflammatory bowel disease IBD intestinal fibrosis inflammation |
| url | https://www.mdpi.com/1422-0067/22/19/10439 |
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