ObjectiveTo summarize the epidemiology of nonalcoholic fatty liver disease (NAFLD) and the epidemiological and economic burdens of NAFLD, so as to provide a reference for hospital management decision-making. MethodThe domestic and foreign guidelines relevant to NAFLD and the literatures relevant to epidemiological investigation and disease burden researches were summarized and its research progress was reviewed. ResultsThe global prevalence of NAFLD was increasing over years. The incidence, mortality, and disability adjusted life years of liver cirrhosis and liver cancer caused by NAFLD had increased year by year. The patients relevant to NAFLD of inpatients and outpatients had increased obviously, and the overall medical expenses had also shown a rising trend. The possible reasons were health care awareness, new drug research, population aging, and excessive medical consumption. In addition, children and adolescents with NAFLD had a obviously increased risk of liver or extrahepatic diseases. ConclusionsBy understanding the epidemiological trend of NAFLD, it is a certain understanding of the disease burden of NAFLD and the related factors affecting the increase of its treatment cost. It is believed that it is necessary to further pay attention to and strengthen the genetic characteristics, pathogenesis, drug research and development, and early diagnosis of cirrhosis and liver cancer relevant to NAFLD in the future. At the same time, the NAFLD group of children and adolescents should not be ignored.
ObjectiveTo understand the current research progress on the role of hydrogen sulfide (H2S) in liver diseases. MethodThe relevant literature on the role of H2S in the liver diseases published in recent years was retrieved and reviewed. ResultsCurrent research focused primarily on exploring the mechanisms of H2S in various liver diseases. Studies had shown that H₂S played an important role in the occurrence and development of liver diseases through mechanisms such as antioxidative stress, anti-inflammatory effects, regulation of autophagy, endoplasmic reticulum stress, angiogenesis, and cell death. ConclusionsBy supplementing exogenous H2S, adjusting the gut microbiota, or inhibiting key enzymes involved in H₂S synthesis, the concentration of H2S in the body can be modulated, providing new strategies for treating liver diseases. However, the related mechanisms are still controversial. Future research should further investigate the specific role of H2S in different liver diseases and how to precisely control its level in the body to achieve targeted drug delivery.