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Articles by Renming Fan
Nanotherapeutic macrophage reprogramming through immunometabolic and microbial modulation for sepsis treatment
Abstract Sepsis is a life-threatening syndrome characterized by dysregulated immune responses and metabolic dysfunction, and remains a major cause of global mortality. While nanomedicine offers new opportunities for sepsis therapy, current strategies rarely achieve comprehensive modulation of macrophage immunometabolism and microenvironmental signaling.
Reprogramming macrophage immunometabolism via glutamine antagonism potentiates colorectal cancer therapy in mice
Abstract Colorectal cancer (CRC) often exhibits a suppressive tumor microenvironment that is associated with elevated glutamine metabolism and induction of immunosuppressive macrophages. Glutamine antagonists such as 6-diazo-5-oxo-L-norleucine (DON) and its prodrug JHU-083 can limit tumor growth, but their toxicity and immune cell selectivity remain suboptimal.
PDE4 modulates muscle signaling in cancer cachexia
Keywords cancer cachexia PDE4 mitochondrial dysfunction Get full text access Log in, subscribe or purchase for full access. References 1. Berriel Diaz, M. ... Cancer cachexia: multilevel metabolic dysfunction Nat. Metab. 2024; 6:2222-2245 2. Wyart, E. ... Systemic metabolic crosstalk as driver of cancer cachexia Trends Endocrinol. Metab. 2025; 36:815-826 3. Ferrer, M. ... Cachexia: a systemic consequence of progressive, unresolved disease Cell. 2023; 186:1824-1845 4. Gicquel, T. ...
Immunometabolic Rewiring of Dendritic Cells to Overcome Glutamine‐Driven Immune Suppression in Colorectal Cancer
1 Introduction Dendritic cells (DCs) are essential mediators of antitumor immunity, functioning as the primary antigen-presenting cells that mediate the link between innate and adaptive immune response.[1] By capturing tumor-associated antigens and presenting them on MHC-I molecules, DCs activate CD8+ cytotoxic T lymphocytes, initiating robust immune responses that are essential for tumor eradication.[2] However, within the tumor microenvironment (TME), DC maturation is often impaired due to...
Degradation of Hexokinase 2 Blocks Glycolysis and Induces GSDME-Dependent Pyroptosis to Amplify Immunogenic Cell Death for Breast Cancer Therapy
Hexokinase 2 (HK2) is the principal rate-limiting enzyme in the aerobic glycolysis pathway and determines the quantity of glucose entering glycolysis. However, the current HK2 inhibitors have poor activity, so we used proteolysis-targeting chimera (PROTAC) technology to design and synthesize novel HK2 degraders. Among them, C-02 has the best activity to degrade HK2 protein and inhibit breast cancer cells.
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