ADM (Adrenomedullin)

The three models are robust and complementary tools for exploring the VCID mechanisms. They have been instrumental in advancing our understanding of VCID pathogenesis and in facilitating the development of novel therapeutic approaches.

Furthermore, histological analysis of patient tissues demonstrated spatial co-localization of GLUT1-expressing TC1 cells with DLL4-positive EC1 cells. These findings elucidate the epigenetic landscape underlying tumor-stromal interactions and establish the ADM/VEGFA axis as a critical therapeutic target to disrupt epigenetically controlled angiogenesis in SNSCC.

ADM depletion attenuated Huh7 cell proliferative capacity, migratory potential, and invasive behavior, reduced xenograft tumor burden in murine models, and substantially potentiated sorafenib antitumor efficacy. This study delineates an ADM-driven TACE-resistant HCC cellular subtype (scPAS+) that functions simultaneously as a prognostic biomarker and actionable therapeutic target for circumventing treatment resistance.

When compared to models inclusive of standalone traditional risk criteria, such as demographic and lifestyle factors, models utilising the protein panels modestly improve prediction for 5 and 10-year mortality (from AUC 0.49-0.57 to AUC of 0.62-0.68). Our results demonstrate the potential of the plasma proteome in risk stratification for all-cause mortality.

The vaccine also proved highly stable at 4 °C, in the absence of cryoprotectants, for more than a month. In summary, we confirmed that a KLH-AM mRNA vaccine is very stable and can elicit humoral and cellular immune responses, inhibit angiogenesis, and delay tumor growth in subcutaneous melanoma, without inducing an immunosuppressive tumor microenvironment (TME), further supporting mRNA vaccines targeting AM as an attractive immunotherapeutic approach.

This macrophage-derived ADM, in turn, accelerates angiogenesis in endothelial cells while enhancing the proliferation and migration of tumor cells. These results elucidate a feedforward loop in the endothelial-BMDM-tumor cell axis, and provide mechanistic insights into the TME of rGBM.

A methionine-restricted diet (MRD) reduced SAM levels, mitigating comorbidity and suppressing tumor growth. Our findings unveil the SAM-METTL14-ADM axis and LPBNGlu → PVTGlu/LHGlu neurocircuits in PDAC-induced brain remodeling, positioning MRD as a promising therapeutic strategy to improve patient outcomes.

These findings collectively suggested that breast cancer cell-derived AM promotes lipid metabolic reprogramming through a Zeb1-dependent manner in CAAs, which displays significant clinical implications and may provide promising therapeutic approaches for targeting the breast cancer-associated adipose microenvironment.

In human GBM tumors and plasmas, ADM correlates positively with GSC stemness, pro-tumor macrophage abundance, and poor prognosis. These findings highlight ADM-triggered GSC-macrophage symbiosis as a promising therapeutic target for GBM.

By leveraging the strengths of both traditional and novel biomarkers, precise therapeutic plans can be developed, thereby improving the management and prognosis of patients with CVDs. The ongoing exploration and validation of these biomarkers are crucial for advancing CV care and addressing the limitations of current diagnostic tools.

In addition, emerging research highlights the role of the gut microbiome in PaC and hyperglycemia. Comprehensive understanding of these mechanisms is critical for early detection and improved treatment strategies for PaC.

In turn, the increased POA in breast cancer competes with arachidonic acid (ARA) for the phospholipid synthesis, leaving more ARA is utilized for PDG2 production to trigger the malignant progression of breast cancer and AM production. Importantly, disruption of Zeb1-dependent lipolytic activity and/or membrane phospholipid remodeling within the TAME dramatically diminishes the aggressiveness of breast cancer in vitro and in vivo.