HMGB1 (High Mobility Group Box 1)

Collectively, we show OLs as an unrecognized source of HMGB1 during oxycodone exposure and establish a novel OL-microglia signaling axis underlying neuroinflammation. These insights emphasize the importance of glial crosstalk in opioid-related pathologies and may inform therapeutic strategies targeting HMGB1 signaling.

Our study revealed a novel mechanism that CAFs conferred osimertinib resistance in NSCLC cells through modulating m7G modification. These findings underscore the importance of m7G modification in the communication between cancer cells and the TME, and pave the way for finding novel therapeutic strategies to overcome drug resistance by targeting m7G modification.

However, TRG therapy restored renal impairments via regulating antioxidative, anti-apoptotic, anti-inflammatory, and histo-architecture. Our findings were strongly supported by in-silico findings that demonstrated the potential binding of TRG with key regulatory genes.

Inflachromene, an inhibitor of the chromatin remodelers HMGB1/2, decoupled mitochondrial bioenergetics from senolytic susceptibility, yielding SASP-null/miR146a-negative senescent cancer cells that were completely resistant to ABT-263/navitoclax and A1331852 despite extensive mitochondrial reprogramming. Thus, the senolytic response is governed by a layered circuit in which mitochondrial bioenergetic heritage establishes the senolytic ceiling, TIS-acquired bioenergetic flexibility fine-tunes the amplitude of the senolytic response, and establishing a mitochondria-inflammatory SASP crosstalk is required for BH3-mediated senolysis. These results support using functional readouts that integrate mitochondrial metabolic flexibility and inflammatory SASP to predict and potentially enhance senolytic efficacy in TIS cancer cells.

In summary, we found that H3K27 acetylation-induced lncRNA-DAPK1-IT1 promotes oxidative stress damage caused by I/R through the miR-25-3p/HMGB1 axis. These findings help to improve our understanding of ischemic stroke and provide new therapeutic avenues.

UV-C radiation and mitomycin C (MMC) were used as positive controls...In contrast, exposure to BQ or DEB promoted strong nuclear retention of HMGB1, consistent with its role in DNA repair. Overall, these findings suggest that, in HCT116 tumor cells, HMGB1 localization is dynamically regulated according to the type and duration of genotoxic stress: physical mutagens favor cytoplasmic signaling responses while chemical mutagens reinforce nuclear repair mechanisms.

This novel mouse model recapitulates native VS progression within the IAC and offers a powerful platform to investigate mechanisms underlying VS-associated SNHL.

ADARB1 exerts its anti-tumor effects primarily through the HMGB1/PFKFB3 pathway. Collectively, these findings identify ADARB1 as a novel tumor suppressor in cervical cancer and a promising therapeutic target for clinical intervention.

HO-1 showed a significant inverse correlation with HMGB-1 (r = -0.405, p = 0.001), KEAP1 was positively correlated with sST2 (r = 0.282, p = 0.029), and GPX4 was correlated with FGF21 (r = 0.255, p = 0.049); no other significant associations were found. β-thalassemia major patients exhibit significant endothelial and cardiac injury markers, altered lipid profiles, and selective upregulation of antioxidant and ferroptosis-related genes.

Collectively, these findings demonstrate that VitD reprograms the immune response to PDT by enhancing cytotoxic immunity while limiting immunosuppressive features. This suggests an immune-priming strategy to consider, possibly alongside immune checkpoint blockade, for treating cutaneous SCC.

Inducing ICD with NPs is a viable therapeutic strategy to potentiate anti-tumor immunity. The convergence of NPs-based ICD inducers with nanotechnology-based delivery systems offers a robust platform for the development of innovative combination regimens aimed at improving patient outcomes.

Future research should focus on elucidating the spatiotemporal dynamics of these mechanisms and integrating immunotherapy with molecular targeting to improve outcomes for PC patients with hepatic metastasis. This review aims to provide a reference for the mechanism research and therapeutic intervention of hepatic metastasis of pancreatic cancer (HMPC).