Hao Shen, Mingjun Yang
This study delineates the shifting paradigms of redox oncology in EC, highlighting a critical transition toward cell death mechanisms and targeted therapeutic validation. Although limited by its restriction to a single database (WoSCC) and English-only publications, these findings provide essential "evidence-based navigation" to optimize resource allocation and foster cross-regional collaborations for precision therapeutic strategies in high-burden regions.
BACKGROUND: Oxidative stress plays a pivotal role in esophageal cancer (EC) pathogenesis, with emerging redox biomarkers-such as the systemic oxidative stress index (SOSI)-demonstrating significant prognostic value in advanced management, including neoadjuvant immunochemotherapy. However, a comprehensive audit of the global research structure and thematic evolution at this intersection remains absent. This study aims to map the intellectual landscapes and paradigm shifts in this evolving field.
METHODS: Literature published between January 1, 1998 and May 13, 2026 was retrieved from the Web of Science Core Collection (WoSCC) using a comprehensive topic search strategy: TS=("esophageal neoplasm" OR "esophageal cancer") AND TS=("oxidative stress" OR "reactive oxygen species" OR "lipid peroxidation"). Only original English research articles were included. Bibliometric parameters and network visualizations were thoroughly evaluated using Microsoft Excel, VOSviewer, CiteSpace, and R software.
RESULTS: A final cohort of 355 original articles exhibited a steady annual growth rate of 7.94%, with China dominating the publication volume (56.9%) and the USA leading international collaborations. The thematic evolution over the past 28 years revealed a profound paradigm shift divided into three distinct stages: transitioning from early toxicological profiling and environmental carcinogen-induced oxidative injuries (e.g., mycotoxins and lipid peroxidation) to histological characterizations, and ultimately culminating in contemporary frontiers centered on novel cell death pathways (ferroptosis, pyroptosis, autophagy) and tumor microenvironment (TME) homeostasis.
CONCLUSIONS: This study delineates the shifting paradigms of redox oncology in EC, highlighting a critical transition toward cell death mechanisms and targeted therapeutic validation. Although limited by its restriction to a single database (WoSCC) and English-only publications, these findings provide essential "evidence-based navigation" to optimize resource allocation and foster cross-regional collaborations for precision therapeutic strategies in high-burden regions.