CX3CL1 (C-X3-C Motif Chemokine Ligand 1)

The review critically evaluates the axis's potential as a biomarker, discusses methodological advances and limitations in human studies, and analyzes therapeutic strategies with a focus on translational challenges. We conclude with a forward-looking perspective on precision medicine approaches targeting this axis.

Mechanistically, CI upregulated the expression of ADAM10, which plays a key role in converting membrane-bound CX3CL1 to its soluble form. This study provided evidence that chronic inflammation could promote tumor progression through the activation of ADAM10/CX3CL1 axis in gastric cancer.

LIFI demonstrated strong discrimination (C statistic, 0.83) and was associated with post-LT infections, longer hospital stays, and reduced patient survival. Per the results of this diagnostic/prognostic study, LIFI identifies LT candidates with severe immune dysfunction at high risk for early post-LT mortality, offering a preoperative, objective tool to refine transplant candidacy, guide perioperative management, and improve LT outcomes.

PLAE is associated with sex-specific dysregulation of the CX3CL1/CX3CR1 axis and convergent neuroimmune-vascular signatures indicative of subclinical endothelial dysfunction. These associative findings support the hypothesis that fractalkine-pathway modulation may mitigate long-term neurobehavioral and cardiovascular vulnerability after PLAE, warranting causal testing.

Targeting CCR5 with genetic knockdown or the approved drug maraviroc impairs GSC stemness and prolongs survival in GBM models. Our work highlights the functional interplay between OLs and GBM cells and positions the CCL5/CCR5 axis as a druggable target in GBM.

We propose that interventions targeting this axis must move beyond traditional agonist/antagonist approaches toward spatiotemporally specific precision control strategies, including intelligent delivery systems, CRISPR-based cell engineering, and AI-driven personalized treatments. Rationally reprogramming the functional orientation of this axis holds promise in overcoming immune checkpoint inhibitor resistance and provides a theoretical foundation for the development of a new generation of cancer immunotherapies.

Our findings highlight the potential of circulating proteins to be biomarkers of TNBC response to NACT. Pre/post-NACT changes in CX3CL1, CXCL5, CD40, ANGPOI-2 and PD-L1 levels suggest their relevance for assessing NACT efficacy. These results will be validated at completion of the INSTIGO trial.

Finally, we propose future research directions: prioritizing patient stratification based on chemokine profiles, developing targeted delivery systems for chemokine antagonists, and combining these approaches with emerging therapies to overcome treatment resistance. This review underscores the critical role of chemokines in OSCC biology and their promising potential to guide the development of novel, effective therapeutic interventions.

The potential target genes of activin A receptor type I (Acvr1), ribosomal protein S6 kinase B1 (Rps6kb1), and transforming growth factor beta receptor type 1 (Tgfbr1) were significantly lower in the kidneys of the LPS group. EVs-derived miR-128-3p in LPS induced periodontitis may cause kidney inflammation which may be mediated by, Rps6kb1, Tgfbr1, and Acvr1.

The shared causal genetic variants between DNER and SCZ suggest a mechanism underlying neuropsychiatric pathogenesis. Further experimental studies are warranted to elucidate the underlying biological mechanisms and identify novel diagnostic biomarkers and therapeutic targets.

Furthermore, it highlights recent progress in therapeutic strategies targeting chemokine axes to mitigate inflammatory bone loss and promote tissue regeneration, while addressing translational barriers including receptor redundancy, context-dependent specificity, and limited in vivo validation. By positioning chemokines as dynamic mediators at the interface of the immune and skeletal systems, this review establishes a conceptual foundation for the development of precision therapeutics aimed at restoring bone homeostasis and treating skeletal disorders.

Within tumor-associated macrophages, DHX34 suppressed CX3CL1 output, limiting the tumor entry of CX3CR1-positive CD8+ T cells and, in turn, impairing control of HCC and reducing responsiveness to checkpoint therapy. Targeting DHX34 may potentiate PD-1 blockade in HCC.