Navigating the metabolic crossroads: A bibliometric analysis of the SLC7A11/xCT field from oxidative stress to ferroptosis and disulfidptosis.

The cystine/glutamate transporter SLC7A11 is a central node in regulated cell death and tumor metabolism. Here, we performed a bibliometric analysis of 4998 publications to map the knowledge structure and temporal evolution of SLC7A11 research, alongside the rapidly expanding disulfidptosis literature. We observed exponential growth post-2012, with a recent surge driven by collaborative networks centered in China with strong links to the United States. Keyword timelines revealed a distinct three-phase trajectory: from foundational redox biology, through a ferroptosis-dominated period, to the emerging concept of disulfidptosis. Currently, ferroptosis remains the core theme in keyword co-occurrence networks, tightly interconnected with oxidative stress, apoptosis, and metabolism. Concurrently, disulfidptosis research is branching into oncology, prognostic modeling, machine learning, the tumor microenvironment (TME), and glucose starvation. Based on these trends, we highlight key translational frontiers, including data-driven patient stratification, spatiotemporal dynamics of the tumor metabolic landscape, and crosstalk among cell death modalities. Crucially, our mapping reveals notable gaps at the interface of disulfidptosis and tumor immunity. Although the immunological implications of disulfidptosis are gaining traction, studies explicitly focused on tertiary lymphoid structures (TLS) are currently absent, and the upstream ncRNA regulatory layer remains underexplored. We propose that nanomedicine-enabled platforms may help bridge disulfidptosis-driven metabolic injury with immune priming and spatial immune organization, while SLC7A11-AS1 regulatory circuits warrant systematic investigation. Together, these findings provide an evidence-informed framework for the precise targeting of SLC7A11-defined metabolic vulnerabilities.