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FXR activation remodels hepatic and intestinal transcriptional landscapes in metabolic dysfunction-associated steatohepatitis.
Wen, Ying-Quan; Zou, Zi-Yuan; Zhao, Guan-Guan; Zhang, Meng-Jiao; Zhang, Yong-Xin; Wang, Gai-Hong; Shi, Jing-Jing; Wang, Yuan-Yang; Song, Ye-Yu; Wang, Hui-Xia; Chen, Ru-Ye; Zheng, Dong-Xuan; Duan, Xiao-Qun; Liu, Ya-Meng; Gonzalez, Frank J; Fan, Jian-Gao; Xie, Cen.
Afiliación
  • Wen YQ; School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.
  • Zou ZY; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Zhao GG; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Zhang MJ; Department of Gastroenterology, Center for Fatty Liver, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Key Lab of Pediatric Gastroenterology and Nutrition, Shanghai, 200092, China.
  • Zhang YX; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Wang GH; Xiangya Hospital, Central South University, Changsha, 410013, China.
  • Shi JJ; School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, 210029, China.
  • Wang YY; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Song YY; University of the Chinese Academy of Sciences, Beijing, 100049, China.
  • Wang HX; Cascade Pharmaceuticals, Inc, Shanghai, 201321, China.
  • Chen RY; Cascade Pharmaceuticals, Inc, Shanghai, 201321, China.
  • Zheng DX; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Duan XQ; Department of Laboratory Medicine and Central Laboratory, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
  • Liu YM; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
  • Gonzalez FJ; Department of Gastroenterology, Center for Fatty Liver, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Key Lab of Pediatric Gastroenterology and Nutrition, Shanghai, 200092, China.
  • Fan JG; Cascade Pharmaceuticals, Inc, Shanghai, 201321, China.
  • Xie C; Cascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Acta Pharmacol Sin ; 45(11): 2313-2327, 2024 Nov.
Article en En | MEDLINE | ID: mdl-38992119
ABSTRACT
The escalating obesity epidemic and aging population have propelled metabolic dysfunction-associated steatohepatitis (MASH) to the forefront of public health concerns. The activation of FXR shows promise to combat MASH and its detrimental consequences. However, the specific alterations within the MASH-related transcriptional network remain elusive, hindering the development of more precise and effective therapeutic strategies. Through a comprehensive analysis of liver RNA-seq data from human and mouse MASH samples, we identified central perturbations within the MASH-associated transcriptional network, including disrupted cellular metabolism and mitochondrial function, decreased tissue repair capability, and increased inflammation and fibrosis. By employing integrated transcriptome profiling of diverse FXR agonists-treated mice, FXR liver-specific knockout mice, and open-source human datasets, we determined that hepatic FXR activation effectively ameliorated MASH by reversing the dysregulated metabolic and inflammatory networks implicated in MASH pathogenesis. This mitigation encompassed resolving fibrosis and reducing immune infiltration. By understanding the core regulatory network of FXR, which is directly correlated with disease severity and treatment response, we identified approximately one-third of the patients who could potentially benefit from FXR agonist therapy. A similar analysis involving intestinal RNA-seq data from FXR agonists-treated mice and FXR intestine-specific knockout mice revealed that intestinal FXR activation attenuates intestinal inflammation, and has promise in attenuating hepatic inflammation and fibrosis. Collectively, our study uncovers the intricate pathophysiological features of MASH at a transcriptional level and highlights the complex interplay between FXR activation and both MASH progression and regression. These findings contribute to precise drug development, utilization, and efficacy evaluation, ultimately aiming to improve patient outcomes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Citoplasmáticos y Nucleares / Ratones Noqueados / Hígado Límite: Animals / Humans / Male Idioma: En Revista: Acta Pharmacol Sin Asunto de la revista: FARMACOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Citoplasmáticos y Nucleares / Ratones Noqueados / Hígado Límite: Animals / Humans / Male Idioma: En Revista: Acta Pharmacol Sin Asunto de la revista: FARMACOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos