Dear Colleagues,
The protein high-mobility group box 1 (HMGB1) plays a crucial role in maintaining cellular homeostasis and regulating the immune response. It was initially described as a nuclear protein that binds to DNA and assists in gene transcription. However, recent studies have revealed extracellular functions as a damage-associated molecular pattern molecule (DAMP) and as a cytokine-like mediator that triggers inflammation and immunity. HMGB1 is released from damaged, stressed, or necrotic cells and can activate various signaling pathways, including TLR4 and RAGE, thereby promoting the expression of pro-inflammatory cytokines and chemokines. It can also induce the differentiation of dendritic cells and macrophages and stimulate the maturation of T and B cells. In addition, HMGB1 can promote tissue repair and regeneration by stimulating angiogenesis and stem cell proliferation. However, dysregulation of HMGB1 can contribute to the development of various diseases, including cancer, autoimmune disorders, neurodegenerative diseases, and infectious diseases. For example, overexpression of HMGB1 is associated with the progression and metastasis of various cancers, whereas the blocking of HMGB1 can inhibit tumor growth and enhance the efficacy of chemotherapy. On the other hand, HMGB1 deficiency or dysfunction can impair immune responses and increase the susceptibility to infections. HMGB1 therefore plays a vital role in maintaining immune homeostasis and promoting tissue repair, but its dysregulation can contribute to various pathological conditions. The targeting of HMGB1 signaling could thus be a promising therapeutic approach for treating inflammatory, autoimmune, and neoplastic diseases. This special issue welcomes contributions that describe the mechanisms by which HMGB1 plays a significant role in the pathogenesis of various diseases, thereby representing a promising target in the development of novel therapies.
Mohmad Farooq Shaikh
Guest Editor
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