Interplay between YAP/TAZ and metabolic dysfunction-associated steatotic liver disease progression.
Autor: | Lee NY; College of Pharmacy, Seoul National University, Seoul, 08826, Korea., Choi MG; College of Pharmacy, Seoul National University, Seoul, 08826, Korea., Lee EJ; College of Pharmacy, Seoul National University, Seoul, 08826, Korea., Koo JH; Research Institute of Pharmaceutical Sciences and Natural Products Research Institute, Seoul National University, Seoul, 08826, Korea. jhkoo@snu.ac.kr. |
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Jazyk: | angličtina |
Zdroj: | Archives of pharmacal research [Arch Pharm Res] 2024 Jun; Vol. 47 (6), pp. 558-570. Date of Electronic Publication: 2024 Jun 14. |
DOI: | 10.1007/s12272-024-01501-5 |
Abstrakt: | Metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming an increasingly pressing global health challenge, with increasing mortality rates showing an upward trend. Two million deaths occur annually from cirrhosis and liver cancer together each year. Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), key effectors of the Hippo signaling pathway, critically regulate tissue homeostasis and disease progression in the liver. While initial studies have shown that YAP expression is normally restricted to cholangiocytes in healthy livers, the activation of YAP/TAZ is observed in other hepatic cells during chronic liver disease. The disease-driven dysregulation of YAP/TAZ appears to be a critical element in the MASLD progression, contributing to hepatocyte dysfunction, inflammation, and fibrosis. In this study, we focused on the complex roles of YAP/TAZ in MASLD and explored how the YAP/TAZ dysregulation of YAP/TAZ drives steatosis, inflammation, fibrosis, and cirrhosis. Finally, the cell-type-specific functions of YAP/TAZ in different types of hepatic cells, such as hepatocytes, hepatic stellate cells, hepatic macrophages, and biliary epithelial cells are discussed, highlighting the multifaceted impact of YAP/TAZ on liver physiology and pathology. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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