PFKFB3 (6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3)

These findings indicated that luteolin ameliorated DIC by targeting PFKFB3 to inhibit EndMT. Luteolin may be a promising adjuvant therapy for mitigating DIC.

RNase R digestion and actinomycin D assays were employed to assess its stability...Animal experiments confirmed that silencing circ_0017521 suppressed tumor growth and glycolysis. This study revealed that hypoxia-induced circ_0017521 activated the PI3K/AKT pathway through the miR-532-3p/PFKFB3 axis, synergistically driving EMT and glycolysis, thereby promoting NSCLC progression.

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.

These findings highlight PKD isoforms as potential therapeutic targets, particularly in cancer settings where metabolic dysfunction plays a contributing role. While current PKD inhibitors lack isoform specificity, future therapeutic strategies focused on PKD2 and PKD3 modulation may offer selective control over invasion, immune evasion, and metabolic reprogramming in metabolically comorbid cancer patients.

In vivo, Daucosterol significantly alleviated CLP-induced ALI by improving lung histopathology, reducing pulmonary edema, enhancing oxygenation, inhibiting myeloperoxidase and caspase-3 activity, and decreasing TNF-α and IL-6 levels in bronchoalveolar lavage fluid. In conclusion, Daucosterol targets PFKFB3 to mitigate sepsis-induced ALI by inhibiting glycolysis and M1 macrophage polarization, offering a potential therapeutic strategy for ALI.

In vivo, NAT10 promoted tumor growth. Collectively, NAT10 contributes to RB progression by enhancing glycolysis through ac4C-mediated PFKFB3 mRNA stabilization, identifying the NAT10-ac4C-PFKFB3 axis as a potential therapeutic target.

PFKFB3 upregulation drives metabolic adaptations that confer resistance to trastuzumab in HER2 + breast cancer. These findings highlight PFKFB3 as a promising therapeutic target to overcome resistance and improve patient outcomes.

PFKFB3 activity was associated with a specific reduction in asparagine availability, potentially pointing to a targeted reprogramming of amino acid metabolism supporting distinct TAM functions under conditions of intra-tumoral metabolic stress. These findings highlight PFKFB3 as an essential regulator of TAMs pro-tumoral metabolism in CRC, particularly in colon cancer.

We conclude that modulation of the metabolic changes associated with immune responses plays an important role in disease progression, and that targeting metabolic checkpoints or kinases may offer promising avenues for future immunotherapy approaches for the treatment of influenza virus infection. We also emphasize the need for further research to develop a comprehensive biological model that clarifies host outcomes and the complex nature of immune-metabolic regulation and crosstalk.

Targeting this shared metabolic-immune-hormonal axis holds immense potential for developing innovative strategies (e.g., metabolic modulators, refined TCM approaches) to improve ER, enhance embryo implantation rates in infertility (including IVF) and recurrent miscarriage, ultimately advancing global reproductive health. Further research is needed to validate core mechanisms.

Simultaneously, isoalloLCA metabolically reprograms macrophages by enhancing oxidative phosphorylation (OXPHOS) that is linked to anti-inflammatory effects. Our research indicates that metabolic modulation of macrophages amplifies the anti-inflammatory properties of isoalloLCA, thereby revealing a promising therapeutic avenue for addressing pediatric IBD.

The comet assay revealed severe DNA damage (Tail DNA, fold change, untreated cell; 1, CUR-20 µM; 1.2, KAN-20 µM; 3, and COMB; 4.6) in the A549 cells, while MMP analysis (color change from red to green) and apoptotic staining confirmed cell death morphologically (color change from green to orange). Moreover, Western blot analysis demonstrated that the combination markedly enhanced apoptosis in the A549 cells.