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HucMSC-Ex alleviates inflammatory bowel disease via the lnc78583-mediated miR3202/HOXB13 pathway / 浙江大学学报(英文版)(B辑:生物医学和生物技术)
Journal of Zhejiang University. Science. B ; (12): 423-431, 2022.
Artículo en Inglés | WPRIM | ID: wpr-929071
ABSTRACT
As a group of nonspecific inflammatory diseases affecting the intestine, inflammatory bowel disease (IBD) exhibits the characteristics of chronic recurring inflammation, and was proven to be increasing in incidence (Kaplan, 2015). IBD induced by genetic background, environmental changes, immune functions, microbial composition, and toxin exposures (Sasson et al., 2021) primarily includes ulcerative colitis (UC) and Crohn's disease (CD) with complicated clinical symptoms featured by abdominal pain, diarrhea, and even blood in stools (Fan et al., 2021; Huang et al., 2021). UC is mainly limited to the rectum and the colon, while CD usually impacts the terminal ileum and colon in a discontinuous manner (Ordás et al., 2012; Panés and Rimola, 2017). In recent years, many studies have suggested the lack of effective measures in the diagnosis and treatment of IBD, prompting an urgent need for new strategies to understand the mechanisms of and offer promising therapies for IBD.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Recurrencia / Cordón Umbilical / Enfermedades Inflamatorias del Intestino / Colitis Ulcerosa / Enfermedad de Crohn / Enfermedad Crónica / Proteínas de Homeodominio / MicroARNs / Diarrea / Células Madre Mesenquimatosas Límite: Humanos Idioma: Inglés Revista: Journal of Zhejiang University. Science. B Año: 2022 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Recurrencia / Cordón Umbilical / Enfermedades Inflamatorias del Intestino / Colitis Ulcerosa / Enfermedad de Crohn / Enfermedad Crónica / Proteínas de Homeodominio / MicroARNs / Diarrea / Células Madre Mesenquimatosas Límite: Humanos Idioma: Inglés Revista: Journal of Zhejiang University. Science. B Año: 2022 Tipo del documento: Artículo