CXCL2 (C-X-C Motif Chemokine Ligand 2)

The LPS group (5 mg/kg, intratracheal) was assigned to either prophylactic regimens (daily saline, dexamethasone 5 mg/kg, or digoxin 1 mg/kg, administered intraperitoneally for 5 days prior to LPS) or therapeutic regimens (same interventions initiated 12 h post-LPS for 3 days). At the study endpoint, pulmonary edema (wet-to-dry ratio) and lung injury pathways were analyzed in lung homogenates, including tumor necrosis factor-alpha (TNF-α), IL-6, myeloperoxidase (MPO), malondialdehyde (MDA), NF-κB (p65) DNA-binding activity, C-X-C motif chemokine ligand 2/macrophage inflammatory protein-2 (CXCL2/MIP-2), and hypoxia-inducible factor-1 alpha (HIF-1α), alongside histopathological evaluations. It also strongly inhibited NF-κB activation, reducing CXCL2/MIP-2, while decreasing HIF-1α in both regimens (each p < 0.001). Histological analysis corroborated these findings, revealing improved alveolar architecture and reduced inflammatory injury. In conclusion, digoxin exhibits potent immunomodulatory activity in experimental ALI, warranting further translational research focused on dose optimization and safety profiling.

Finally, PL treatment significantly inhibited in vivo tumor growth and suppressed CAF infiltration in the tumor microenvironment. Together, these findings demonstrated that PL might be a promising chemotherapeutic agent to efficiently target YAP-ET-1-CXCL2 signaling and thus has therapeutic potential for TNBC patients.

P=N/A, N=300, Enrolling by invitation, Mayo Clinic | Trial completion date: Dec 2025 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2028

Collectively, these findings indicate that as CRC advances, increased secretion of CXCL2 from malignant cells stimulates ACKR1 on ECs, thereby promoting tumor invasion and metastasis. This study provides a framework for stage-specific interventions, particularly for locally advanced CRC, by disrupting ACKR1 on ECs within TME to impede metastasis and improve clinical outcomes.

Consequently, this reduces the transcription of sterol regulatory element binding transcription factor 2 (SREBF2) and suppresses cholesterol biosynthesis, thereby remodeling HCC microenvironment and impeding HCC development. In summary, this study highlights the unconventional role of CXCL2 in regulating neutrophil polarization and immune responses in HCC, positioning it as a potential therapeutic target for HCC.

Our findings demonstrate that CAV1 exerts its anti-tumor effects, at least in part, by inhibiting EGFR degradation and modulating the AKT/STAT3 pathway, as well as enhancing the Bax/Caspase-3/Bcl-2 signaling pathway in LUAD cells. These results suggest that targeting CAV1 may represent a promising therapeutic strategy for the treatment of LUAD patients.

In rescue assays, CXCL2 overexpression counteracted the restrictive impact of Fli1 deficiency on LPS-induced HPMEC apoptotic behaviors and inflammatory response. The Fli1 transcription factor aggravates LPS-induced HPMEC dysfunction via binding to CXCL2 promoter in septic ALI.

This study demonstrates that GAL3 enhances the immunosuppressive function of MDSCs in CC, leading to impaired CD8+ T cells function and poor patient prognosis. These findings identify GAL3 and MDSCs as promising targets for therapeutic intervention, providing a basis for novel immunotherapeutic approaches in CC treatment.

These findings reveal a mechanism by which Caspase-6/GSDMC-mediated tumor cell pyroptosis, in response to hypoxic and low-glucose conditions, remodels the immunosuppressive microenvironment through CXCL2-dependent recruitment of MDSCs. These results identify GSDMC as a potential drug target for CRC therapy.

Dengue fever with hepatic involvement is related to serum sTM and sP-selectin levels, thus suggesting that platelet and endothelial cell activation may be involved in the pathogenesis of liver damage and can be used as early predictors of dengue liver damage.

Furthermore, the role of CXCL2 encompasses inflammatory conditions like lung inflammation, atherosclerosis, and obesity. This article examines the structural characteristics, biological roles, and molecular foundation of CXCL2 in carcinogenesis and inflammatory disorders.

This study highlights TNFAIP3, CXCL2, NEDD4L, and SESN2 as candidate genes associated with ferroptosis during LIRI, with SESN2 potentially protecting against PGD. These findings offer promising therapeutic targets for preventing LIRI and improving outcomes in lung transplantation.