The proximal part of the small intestine, including duodenum and jejunum, is not only dedicated to nutrient digestion and absorption but is also a highly regulated immune site exposed to environmental factors. Host-protective responses against pathogens and tolerance to food antigens are essential functions in the small intestine. The cellular ecology and molecular pathways to maintain those functions are complex. Maladaptation is highlighted by common immune-mediated diseases such as coeliac disease, environmental enteric dysfunction or duodenal Crohn’s disease. An expanding spectrum of more than 100 rare monogenic disorders inform on causative molecular mechanisms of nutrient absorption, epithelial homeostasis and barrier function, as well as inflammatory immune responses and immune regulation. Here, after summarizing the architectural and cellular traits that underlie the functions of the proximal intestine, we discuss how the integration of tissue immunopathology and molecular mechanisms can contribute towards our understanding of disease and guide diagnosis. We propose an integrated mechanism-based taxonomy and discuss the latest experimental approaches to gain new mechanistic insight into these disorders with large disease burden worldwide as well as implications for therapeutic interventions. The proximal small intestine is key for nutrition, metabolism and immune responses, and can be affected by a wide range of disorders. This Review describes the cellular and molecular bases of diseases of the proximal small intestine (including rare monogenic disorders), proposing a mechanism-based taxonomy.
{"title":"Cellular and molecular basis of proximal small intestine disorders","authors":"Tania Bildstein, Fabienne Charbit-Henrion, Aline Azabdaftari, Nadine Cerf-Bensussan, Holm H. Uhlig","doi":"10.1038/s41575-024-00962-9","DOIUrl":"10.1038/s41575-024-00962-9","url":null,"abstract":"The proximal part of the small intestine, including duodenum and jejunum, is not only dedicated to nutrient digestion and absorption but is also a highly regulated immune site exposed to environmental factors. Host-protective responses against pathogens and tolerance to food antigens are essential functions in the small intestine. The cellular ecology and molecular pathways to maintain those functions are complex. Maladaptation is highlighted by common immune-mediated diseases such as coeliac disease, environmental enteric dysfunction or duodenal Crohn’s disease. An expanding spectrum of more than 100 rare monogenic disorders inform on causative molecular mechanisms of nutrient absorption, epithelial homeostasis and barrier function, as well as inflammatory immune responses and immune regulation. Here, after summarizing the architectural and cellular traits that underlie the functions of the proximal intestine, we discuss how the integration of tissue immunopathology and molecular mechanisms can contribute towards our understanding of disease and guide diagnosis. We propose an integrated mechanism-based taxonomy and discuss the latest experimental approaches to gain new mechanistic insight into these disorders with large disease burden worldwide as well as implications for therapeutic interventions. The proximal small intestine is key for nutrition, metabolism and immune responses, and can be affected by a wide range of disorders. This Review describes the cellular and molecular bases of diseases of the proximal small intestine (including rare monogenic disorders), proposing a mechanism-based taxonomy.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 10","pages":"687-709"},"PeriodicalIF":45.9,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141904647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-05DOI: 10.1038/s41575-024-00972-7
Eleni Kotsiliti
{"title":"Metastatic pancreatic cancer and the liver","authors":"Eleni Kotsiliti","doi":"10.1038/s41575-024-00972-7","DOIUrl":"10.1038/s41575-024-00972-7","url":null,"abstract":"","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 9","pages":"606-606"},"PeriodicalIF":45.9,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-05DOI: 10.1038/s41575-024-00976-3
Juan M. Pericàs, Quentin M. Anstee, Salvador Augustin, Ramón Bataller, Annalisa Berzigotti, Andreea Ciudin, Sven Francque, Juan G. Abraldes, Virginia Hernández-Gea, Mònica Pons, Thomas Reiberger, Ian A. Rowe, Peter Rydqvist, Elmer Schabel, Frank Tacke, Emmanuel A. Tsochatzis, Joan Genescà
{"title":"Author Correction: A roadmap for clinical trials in MASH-related compensated cirrhosis","authors":"Juan M. Pericàs, Quentin M. Anstee, Salvador Augustin, Ramón Bataller, Annalisa Berzigotti, Andreea Ciudin, Sven Francque, Juan G. Abraldes, Virginia Hernández-Gea, Mònica Pons, Thomas Reiberger, Ian A. Rowe, Peter Rydqvist, Elmer Schabel, Frank Tacke, Emmanuel A. Tsochatzis, Joan Genescà","doi":"10.1038/s41575-024-00976-3","DOIUrl":"10.1038/s41575-024-00976-3","url":null,"abstract":"","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 11","pages":"824-824"},"PeriodicalIF":45.9,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41575-024-00976-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-29DOI: 10.1038/s41575-024-00959-4
Shira Zelber-Sagi, Patrizia Carrieri, Juan M. Pericàs, Dana Ivancovsky-Wajcman, Zobair M. Younossi, Jeffrey V. Lazarus
Liver disease prevalence, severity, outcomes and hepatic risk factors (for example, unhealthy diet) are heavily affected by socioeconomic status and food insecurity. Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent liver disease globally and is likely to co-occur with other liver diseases associated with food insecurity. Though weight reduction and adopting a healthy diet can reverse the course of MASLD, gaps between recommendations and practice transcend individual responsibility and preference. Broader sociocultural determinants of food choices (social nutrition) include food insecurity, community and social norms and the local environment, including commercial pressures that target people experiencing poverty, ethnic minorities and children. Food insecurity is a barrier to a healthy diet, as a low-quality diet is often less expensive than a healthy one. Consequently, food insecurity is an ‘upstream’ risk factor for MASLD, advanced fibrosis and greater all-cause mortality among patients with liver disease. Intervening on food insecurity at four major levels (environment, policy, community and health care) can reduce the burden of liver disease, thereby reducing social and health inequities. In this Review, we report on the current research in the field, the need for implementing proven interventions, and the role liver specialists can have. Metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence is increasing worldwide, and a crucial risk factor is food insecurity. This Review provides an extensive overview of food insecurity in the context of MASLD and discusses potential policies and procedures as interventions.
{"title":"Food inequity and insecurity and MASLD: burden, challenges, and interventions","authors":"Shira Zelber-Sagi, Patrizia Carrieri, Juan M. Pericàs, Dana Ivancovsky-Wajcman, Zobair M. Younossi, Jeffrey V. Lazarus","doi":"10.1038/s41575-024-00959-4","DOIUrl":"10.1038/s41575-024-00959-4","url":null,"abstract":"Liver disease prevalence, severity, outcomes and hepatic risk factors (for example, unhealthy diet) are heavily affected by socioeconomic status and food insecurity. Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent liver disease globally and is likely to co-occur with other liver diseases associated with food insecurity. Though weight reduction and adopting a healthy diet can reverse the course of MASLD, gaps between recommendations and practice transcend individual responsibility and preference. Broader sociocultural determinants of food choices (social nutrition) include food insecurity, community and social norms and the local environment, including commercial pressures that target people experiencing poverty, ethnic minorities and children. Food insecurity is a barrier to a healthy diet, as a low-quality diet is often less expensive than a healthy one. Consequently, food insecurity is an ‘upstream’ risk factor for MASLD, advanced fibrosis and greater all-cause mortality among patients with liver disease. Intervening on food insecurity at four major levels (environment, policy, community and health care) can reduce the burden of liver disease, thereby reducing social and health inequities. In this Review, we report on the current research in the field, the need for implementing proven interventions, and the role liver specialists can have. Metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence is increasing worldwide, and a crucial risk factor is food insecurity. This Review provides an extensive overview of food insecurity in the context of MASLD and discusses potential policies and procedures as interventions.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 10","pages":"668-686"},"PeriodicalIF":45.9,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41575-024-00959-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-28DOI: 10.1038/s41575-024-00956-7
Yvonne A. Nartey, Ansumana S. Bockarie
Mother-to-child transmission of hepatitis B virus remains a mode of transmission in high-burden regions where there are gaps in antenatal screening, limited hepatitis B virus birth-dose vaccination and variable access to antiviral prophylaxis. Policymakers, governments and relevant stakeholders must ensure equitable access to necessary interventions to achieve elimination targets.
{"title":"Mother-to-child transmission of hepatitis B: current status and the road forward","authors":"Yvonne A. Nartey, Ansumana S. Bockarie","doi":"10.1038/s41575-024-00956-7","DOIUrl":"10.1038/s41575-024-00956-7","url":null,"abstract":"Mother-to-child transmission of hepatitis B virus remains a mode of transmission in high-burden regions where there are gaps in antenatal screening, limited hepatitis B virus birth-dose vaccination and variable access to antiviral prophylaxis. Policymakers, governments and relevant stakeholders must ensure equitable access to necessary interventions to achieve elimination targets.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 8","pages":"531-532"},"PeriodicalIF":45.9,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141769163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-28DOI: 10.1038/s41575-024-00963-8
The countdown to the 2030 viral hepatitis elimination goal continues, but time is running out and progress is not keeping pace. Viral hepatitis remains a major public health challenge; we need to take action now to mobilize resources and focus efforts.
{"title":"Viral hepatitis elimination — time to act","authors":"","doi":"10.1038/s41575-024-00963-8","DOIUrl":"10.1038/s41575-024-00963-8","url":null,"abstract":"The countdown to the 2030 viral hepatitis elimination goal continues, but time is running out and progress is not keeping pace. Viral hepatitis remains a major public health challenge; we need to take action now to mobilize resources and focus efforts.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 8","pages":"529-529"},"PeriodicalIF":45.9,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41575-024-00963-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141769164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-24DOI: 10.1038/s41575-024-00964-7
Mathijs P. Verhagen, Mark Schmitt, Riccardo Fodde
Western lifestyles cause a low-grade but chronic and metabolic inflammation (or metaflammation), which might prime committed cell lineages to initiate colon tumorigenesis. At-risk individuals might include cases of early-onset colon cancer, the incidence of which has risen dramatically in the past few decades.
{"title":"Western lifestyle, metaflammation and the cell of origin of colon cancer","authors":"Mathijs P. Verhagen, Mark Schmitt, Riccardo Fodde","doi":"10.1038/s41575-024-00964-7","DOIUrl":"10.1038/s41575-024-00964-7","url":null,"abstract":"Western lifestyles cause a low-grade but chronic and metabolic inflammation (or metaflammation), which might prime committed cell lineages to initiate colon tumorigenesis. At-risk individuals might include cases of early-onset colon cancer, the incidence of which has risen dramatically in the past few decades.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":"21 9","pages":"603-604"},"PeriodicalIF":45.9,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141754747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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