World Hepatitis Day, 28 July, is an opportunity to step up international focus on hepatitis, highlighting the need for a greater global response to liver diseases.
HMGB1 protein, known for its involvement in inflammatory responses, plays significant roles in conditions such as liver ischemia-reperfusion (LI/R) injury and Hepatitis B virus (HBV) infection.
HMGB1 and Liver Ischemia-Reperfusion Injury
Liver ischemia-reperfusion injury, a condition often occurring during liver surgeries and transplants, involves two phases: local ischemia that damages hepatic cells and a subsequent inflammatory response that exacerbates the injury. HMGB1, as a damage-associated molecular pattern (DAMP) molecule, is central to this process.
Recent studies have shown that HMGB1 secretion from hepatocytes is mediated by a process known as lactylation, which occurs during glycolysis. Research indicates that Heat Shock Protein A12A (HSPA12A) can inhibit this lactylation process, thereby reducing HMGB1 secretion and subsequent macrophage chemotaxis and inflammation. This highlights the therapeutic potential of targeting HSPA12A to mitigate liver damage caused by ischemia-reperfusion injury.
HMGB1 and Hepatitis B Virus (HBV) Infection
The HBV X protein (HBx) counteracts HMGB1-mediated epigenetic silencing of covalently closed circular DNA (cccDNA), which is essential for viral persistence and replication. HBx prevents HMGB1 from binding to cccDNA, thus maintaining the cccDNA in a transcriptionally active state. This interaction between HBx and HMGB1 is crucial for the continued replication of HBV within the liver cells.
Targeting HMGB1 directly or modulating its interactions and modifications could lead to innovative treatments for liver ischemia-reperfusion injury and HBV infection. In the month of World Hepatitis Day, we recognize the ongoing research efforts and the potential for HMGB1-targeted therapies to improve liver health outcomes globally.
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Read the full articles about the studies:
https://pubmed.ncbi.nlm.nih.gov/37441587
https://pubmed.ncbi.nlm.nih.gov/35679251
