GDF15 (Growth differentiation factor 15)

This study delineated transcriptional differences between primary tumors and MetLNs in lung cancer, thereby providing a foundation for further exploration of LN metastasis.

GDF-15 >1,400 pg/mL independently predicted adverse outcomes (HR 2.03, p = 0.046). GDF-15 and suPAR provide incremental prognostic value for short-term risk stratification after transcatheter tricuspid valve intervention.

The disruption of this feedforward loop with GDF15-neutralizing antibody, anti-CSF1R antibody, or Rearranged during Transfection (RET) inhibitor markedly reduces both cachexia and anorexia. These findings reveal a non-cell-autonomous mechanism linking tumor signals, macrophage-derived GDF15, and neural pathways, highlighting the tumor-immune-neural triad as a promising therapeutic target.

Silencing METTL3 inhibits the malignant biological progression of PCa by mediating GDF15 via a YTHDF1-dependent m6A mechanism. It is important to further research GDF15 and reveal its specific mechanism in PCa.

TGFBI knockdown or GDF15 inhibition results in a decrease in functional proteins associated with stemness maintenance, which suppresses bladder CSCs' self-renewal and effectively improves the efficacy of chemotherapy. Together, these findings demonstrate the pivotal role of TGFBI in BLCA's stemness maintenance and BLCA progression, highlighting that the inhibition of the TGFBI/GDF15 axis is a potential therapeutic strategy for the amelioration of cancer chemotherapy.

Finally, we translate the framework into actionable hypotheses for EV-informed endotyping, biomarker development (including stool EV assays), and therapeutic strategies targeting shared signaling nodes (e.g., TLR4-p38) and endocrine mediators that are predominantly soluble but may be fractionally vesicle-associated (e.g., GDF15). By reframing CRC cachexia as an emergent property of tumor-host-microbiota vesicular communication, this review provides a roadmap for mechanistic studies and clinically tractable interventions.

Our findings demonstrate that GDF15 acts as a tumor promoter in CRC by driving EMT, facilitating proliferation and metastasis, and enhancing cancer stemness. This study identifies GDF15 as a potential biomarker and therapeutic target for CRC.

These effects position GDF-15 as a key node linking mechanical stress, co-operation with inflammatory factors, abnormal vascular development, and immune dysfunction, thereby converging on a pathways and processes not previously described in melanomas. Uncovering GDF-15 as a central mediator at the intersection of mechanical rigidity and external force, disorganized vascular hemorrhagic remodeling, co-operation with inflammatory factors, and immune evasion, revealing a previously unrecognized therapeutic vulnerability across both common and rare melanoma subtypes.

Male sex was associated with a higher risk of kidney failure and mortality, despite adjustment for demographic, clinical, and treatment factors. Males had higher levels of inflammatory and extracellular matrix deposition biomarkers. In contrast, females showed higher levels of matrix turnover and degradation markers. After adjustment for these biomarker differences, the elevated risk associated with male sex was eliminated, suggesting a biological basis for the observed sex difference in outcomes.

This combination therapy, by addressing multiple pathogenic pathways simultaneously, could potentially be beneficial in patients with cardiovascular risk conditions. In conclusion, the combination of ZOFE and NEBI offers a potentially promising therapeutic approach for managing hypertension and protecting vascular health, aiming at improving clinical outcomes for patients with cardiovascular diseases.