AMPK (Protein Kinase AMP-Activated Catalytic Subunit Alpha 1)

This review provides a comprehensive synthesis of the sources, pharmacological actions, safety, pharmacokinetics, and potential applications of GS. Future research should focus on structural modification of GS, development of novel formulations, and exploration of synergistic combinations with other therapeutic agents to broaden its clinical utility.

Distinct epigenetic signatures associated with AMPK regulation are being explored as a potential therapeutic target. This review provides a comprehensive overview of epigenetic regulation of AMPK in cancer and highlights its potential in the context of metabolic reprogramming and precision oncology.

Emerging technologies such as spatial metabolomics and single-cell multi-omics are now enabling the identification of patient-specific metabolic dependencies. Targeting metabolic symbiosis rather than isolated pathways represents a promising direction for precision oncology, offering opportunities to disrupt tumor stroma cooperation, overcome therapeutic resistance, and personalize metabolism-based interventions.

Protein ubiquitination was higher in alcohol-treated females but not males. Overall, male and female mice displayed divergent responses relative to their same sex controls in response to alcohol consumption before and during cancer.

We argue that effective targeting of the autophagy-senescence axis requires precision gerontology, integrating dynamic biomarkers to guide stage-specific interventions-autophagy activation for prevention and autophagy inhibition or senolysis for established disease. This threshold-based perspective provides a rational foundation for next-generation therapeutic strategies targeting aging and age-related disorders.

Clinical studies, however, have yielded mixed results, underscoring the complexity of metformin's effects and the need for rigorous investigation. This review highlights the multifaceted mechanisms by which metformin impacts tumor progression and discusses its promise and challenges as a therapeutic agent in cancer prevention and treatment.

Recently developed technologies such as CRISPR-based functional genomics, metabolomics, and AI-powered modeling represent new-age tools in defining ferroptosis networks and precision therapeutics design. Integration of the regulation of normal physiological ferroptosis into cancer and diabetes therapy has the potential to redefine redox-targeted therapy and metabolic medicine. Antioxid. Redox Signal. 00, 000-000.

Moringa oleifera Lam. exhibits strong cardioprotective potential, and nanoformulation-based delivery systems further augment its therapeutic efficacy. While preclinical evidence is encouraging, rigorously designed clinical studies are urgently required to validate its safety, effectiveness, and translational value in CVD management.

In vivo studies support these findings, showing increased FoxO3a and decreased survivin in brain tissue sections from metformin-treated mice compared with untreated controls. These results suggest new possibilities for repurposing MET as an adjuvant treatment for GB.

This review provides a detailed theoretical basis for the pathology and treatment of UC. Future research could focus on optimizing the treatment plan and achieving more precise and personalized treatment with multiple targets in multiple aspects.

Although dexrazoxane is the only FDA-approved cardioprotective agent, concerns about its long-term safety and potential interference with doxorubicin's antitumor effectiveness have increased the search for safer alternatives. Despite promising preclinical evidence of their antioxidant, anti-inflammatory, and anti-apoptotic properties, the clinical use of phytochemicals is limited by issues such as low bioavailability, poor specificity, dose-dependent toxicity, variable pharmacokinetics, and lack of standardisation. Therefore, innovative approaches-such as ligand-targeted delivery systems, nanotechnology-based formulations, and structural modifications of lead compounds-are essential to enhance their pharmacological properties, safety, and therapeutic effectiveness for effective cardioprotection against doxorubicin-induced toxicity.