International Journal of Pharmaceutics, Год журнала: 2024, Номер unknown, С. 125058 - 125058
Опубликована: Дек. 1, 2024
Язык: Английский
European Journal of Pharmacology, Год журнала: 2025, Номер 996, С. 177344 - 177344
Опубликована: Фев. 25, 2025
Язык: Английский
Процитировано
0
Annals of Hepatology, Год журнала: 2025, Номер unknown, С. 101896 - 101896
Опубликована: Март 1, 2025
Liver fibrosis is a progressive response to chronic liver diseases characterized by wound-healing process that leads the accumulation of fibrillary extracellular matrix (ECM) proteins in and around tissue. If left untreated, can advance cirrhosis ultimately result failure. Although there have been significant advancements understanding molecular mechanisms involved fibrosis, effective therapeutic strategies reverse or halt condition remain limited. Recent research has underscored critical role energy metabolism initiation progression fibrosis. In injury, hepatic cells undergo metabolic reprogramming meet demands myofibroblasts. This involves various changes, including mitochondrial dysfunction, alterations cellular bioenergetics, shifts glycolysis oxidative phosphorylation, as well changes lipid metabolism. These modifications disrupt homeostasis increase release, activating cells, primarily stellate (HSCs). Activated HSCs then stimulate fibrogenic pathways, leading ECM liver, which exacerbates review aims explore emerging connection between focusing on drive this condition. We also examine implications modulating reduce release mitigate Altering decrease may represent promising approach for treating diseases.
Язык: Английский
Процитировано
0
Cellular Signalling, Год журнала: 2024, Номер 122, С. 111302 - 111302
Опубликована: Июль 25, 2024
Язык: Английский
Процитировано
1
International Journal of Pharmaceutics, Год журнала: 2024, Номер unknown, С. 125058 - 125058
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
0