Ferroptosis, an iron-dependent form of regulated cell death, is driven by lipid peroxidation and shaped by metabolic and antioxidant pathways. In immune cells, ferroptosis susceptibility varies by cell types, lipid composition, and metabolic demands, influencing immune responses in cancer, infections, and autoimmune diseases. Therapeutically, targeting ferroptosis holds promise in cancer immunotherapy by enhancing antitumor immunity or inhibiting immunosuppressive cells. This review highlights the metabolic pathways underlying ferroptosis, its regulation in immune cells, its dual role in tumor progression and antitumor immunity, and its context-dependent therapeutic implications for optimizing cancer treatment.
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http://dx.doi.org/10.4110/in.2025.25.e6 | DOI Listing |
FASEB J
March 2025
Department of Oncology, The Central Hospital of Yongzhou, Yongzhou, Hunan, China.
The ribophorin family, including RPN1, has been associated with tumor progression, but its specific role in pan-cancer dynamics remains unclear. Using data from TCGA, GTEx, and Ualcan databases, we investigated the relationship of RPN1 with prognosis, genomic alterations, and epigenetic modifications across various cancers. Differential analysis revealed elevated RPN1 expression in multiple cancer types, indicating a potential prognostic value.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
March 2025
Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research, Quebec, Canada (O.B., P.P., E.L.S.).
Hypertension is associated with vascular injury characterized by vascular dysfunction, remodeling, and stiffening, which contributes to end-organ damage leading to cardiovascular events and potentially death. Innate (macrophages and dendritic cells), innate-like (γδ T cells) and adaptive immune cells (T and B cells) play a role in hypertension and vascular injury. Perivascular adipose tissue that is the fourth layer of the blood vessel wall is an important homeostatic regulator of vascular tone.
View Article and Find Full Text PDFClin Exp Immunol
March 2025
School of Medicine, Guizhou University, Guiyang 550025, China.
Introduction: Immunotherapy has rapidly become a primary treatment option for many lung cancer patients because of its success in treating this prevalent and deadly disease. However, the success of immunotherapy relies on overcoming the immunosuppressive tumour microenvironment, making remodelling this environment a potential strategy for lung cancer therapy. Research suggests that Toll-like receptor (TLR) agonists can impede tumour growth by promoting the conversion of tumour-associated macrophages into an M1-like state or enhancing dendritic cell development.
View Article and Find Full Text PDFAdv Healthc Mater
March 2025
Department of Ultrasound, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361000, P. R. China.
The abnormal tumor mechanical microenvironment due to specific cancer-associated fibroblasts (CAFs) subset and low tumor immunogenicity caused by inefficient conversion of active chemotherapeutic agents are two key obstacles that impede patients with desmoplastic tumors from achieving stable and complete immune responses. Herein, it is demonstrated that FAP-αCAFs-induced stromal stiffness accelerated tumor progression by precluding cytotoxic T lymphocytes. Subsequently, a cascade-responsive nanoprodrug capable of re-educating FAP-αCAFs and amplifying tumor immunogenicity for potentiated cancer mechanoimmunotherapy is ingeniously designed.
View Article and Find Full Text PDFHaematologica
March 2025
Experimental Hematology, Vall d'Hebron Institute of Oncology (VHIO), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona, Bellaterra.
Continuous treatment with ibrutinib not only exerts tumor control but also enhances T cell function in patients with chronic lymphocytic leukemia (CLL). We conducted longitudinal multi-omics analyses in samples from CLL patients receiving ibrutinib upfront to identify potential adaptive mechanisms to Bruton tyrosine kinase (BTK) inhibition during the first 12 months of continuous therapy. We found that ibrutinib induced a decrease in the expression of exhaustion markers and the proportion of Tregs and Tfh cells normalized to levels observed in healthy donors.
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