Does the pathophysiology of hepatocytes in NASH lead to alterations in the function of kupffer cells?4 answersThe pathophysiology of hepatocytes in Non-alcoholic Steatohepatitis (NASH) can indeed lead to alterations in the function of Kupffer cells (KCs). In NASH, resident KCs are progressively lost and replaced by monocyte-derived macrophages (MdMs). The loss of KCs contributes to disease pathology in NASH, as shown by the preservation of KC number in a mouse model with TFEB overexpression, leading to reduced inflammation and liver injury. Single-cell RNA sequencing identified changes in KC subsets during NASH, with specific subsets like Vsig4+ KCs being protective against NASH by improving hepatic inflammation and fibrosis. The crosstalk between hepatocytes and KCs plays a crucial role in the pathogenesis of NASH, highlighting the intricate relationship between these cell types in the progression of the disease.
What is the mechanism of liver inflammation in COVID-19?5 answersLiver inflammation in COVID-19 is primarily caused by the aggressive cytokine storm induced by the SARS-CoV-2 virus. This cytokine storm leads to cytotoxicity in various organs, including the liver. Additionally, hepatocytes undergo apoptosis or necrosis, releasing pro-inflammatory and pro-fibrogenic mediators that contribute to chronic liver inflammation. The inflammatory response in COVID-19 is characterized by the expression of proinflammatory cytokines such as IL-1β, IL-6, IL-8, IL-18, MCP-1, and TNFα, which significantly impair liver function. The direct cytopathic effects of the virus, host reaction, hypoxia, drugs, and vaccination may also contribute to liver injury in COVID-19. Furthermore, the activation of the NLRP3 inflammasome, a key regulator of inflammation, is closely associated with liver inflammation in COVID-19 and other liver diseases. Inhibition of the NLRP3 inflammasome signaling pathway may offer a potential therapeutic strategy for treating liver inflammation in COVID-19.
How is endoplasmic reticulum stress related to inflammatory bowel disease?5 answersEndoplasmic reticulum stress (ERS) is closely related to inflammatory bowel disease (IBD). ERS is a condition where unfolded or misfolded proteins accumulate in the endoplasmic reticulum, leading to cellular damage. Several studies have shown that ERS plays a vital role in promoting inflammatory response in IBD. The activation of ERS in IBD is associated with increased expression of GRP78, an ER stress indicator, in the intestinal tissues of IBD patients. Additionally, ERS has been found to upregulate the expression and secretion of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-8. Furthermore, ERS-induced inflammation in IBD may be mediated by the activation of p38 MAPK signaling pathway. These findings suggest that ERS plays a significant role in the pathogenesis of IBD and could be a potential therapeutic target for the disease.
What is the role of TLR4 in the development of liver inflammation?4 answersTLR4 plays a crucial role in the development of liver inflammation. Activation of the TLR4-related signaling axis promotes disease progression in liver-related diseases, including acute liver injury, viral hepatitis, alcoholic and non-alcoholic liver disease, cirrhosis, and liver cancer. Chronic intermittent hypoxia (CIH) induces hepatic fibrosis through the TLR4/NF-κB/MAPK signaling pathway. In a rat model of periodontitis-induced hepatic injury, the TLR4/MyD88/NF-κB pathway was found to be involved in liver inflammation. TLR4 participates in and regulates acetaminophen (APAP)-induced liver injury through the JNK signaling pathway. Silencing TLR4 attenuates lipopolysaccharide (LPS)-induced liver injury by inhibiting inflammation and apoptosis via the TLR4/MyD88/NF-κB signaling pathway. Overall, these findings highlight the important role of TLR4 in liver inflammation and suggest that targeting the TLR4 pathway may have therapeutic implications for liver-related diseases.
How do you get rid of inflammation of the liver?10 answers
How to decrease inflammation in liver?10 answers