Inflammation and oxidative stress are the key pathogenic mechanisms for the occurrence and development of liver fibrosis. After liver cell damage, excessive reactive oxygen species (ROS) are released, which is a key trigger for the activation of hepatic stellate cells (HSCs). Once activated, HSCs transform into myofibroblasts, leading to excessive extracellular matrix (ECM) deposition and promoting the formation of liver fibrosis. The above processes interact with each other, mutually amplifying and forming a vicious cycle, jointly accelerating the development process of liver fibrosis. The commonly used antioxidants in clinical practice, such as SOD, CAT, and anthocyanins, play a significant role in clinical antioxidant therapy. Vitamins, as common and natural antioxidants, have the characteristic of being both food and medicine, and are relatively safe. Compared with the commonly used antioxidants in clinical settings, vitamins have higher bioavailability, lower adverse reactions and side effects, are widely available, and are easy to obtain. Patients with liver fibrosis often suffer from multiple vitamin deficiencies due to reduced intake, absorption disorders, and increased consumption. This may further accelerate the disease progression. However, the anti-inflammatory and antioxidant effects of vitamins in liver fibrosis and their underlying mechanisms have not been fully elucidated. Moreover, systematic studies on various vitamins are still relatively scarce. Based on the above background, this article systematically elaborates on the research progress of various vitamins in the prevention and treatment of liver fibrosis through their antioxidant and anti-inflammatory mechanisms, with a focus on correcting the deficiency state. The aim is to provide a theoretical basis for precise nutritional intervention for patients with liver fibrosis due to vitamin deficiency.
Feng et al. (Fri,) studied this question.