Interleukin signaling and iron dysregulation in SARS-CoV-2 pathogenesis and therapeutic targeting

It is crucial for individuals with high Fe levels to closely monitor their symptoms and seek medical attention if needed. This review article offers a brief yet valuable overview of how inflammation can be managed and immune cells can be activated using IL and their interactions with ACE2, TMPRSS2, and FURIN protease. It also discusses the therapeutic potential of drugs as anti-COVID agents in patients with Fe overload, presenting a new avenue for treating SARS-CoV-2 effectively. The search primarily targeted peer-reviewed English-language articles, including clinical trials and scientific reviews. Researches published through 1983 and 2025 were compiled from reference lists and different electronic databases. IL is vital for controlling inflammation and activating immune cells, playing a crucial role in coordinating the body’s immune response to infections and diseases. In patients with SARS-CoV-2 infection, regulating Fe levels through ACE2, TMPRSS2, or FURIN using pharmacological practices could be a suitable therapeutic approach to control this virus. Cytokine signaling (IL-1 to IL-6), Fe metabolism controlled by the hepcidin–ferroportin axis, immune checkpoint pathways (PD-1/PD-L1), and viral entry factors (ACE2, TMPRSS2, and FURIN) all interact intricately in COVID-19 immunopathology, which offers a conceptual framework for comprehending the complex mechanisms causing illness development and locating possible therapy targets.