Abstract
Endocrine-disrupting chemicals (EDCs), ubiquitous in the environment, are increasingly recognized for their detrimental effects on human health. Chronic exposure to EDCs disrupts essential physiological systems, particularly those regulating reproductive, neurological, and metabolic homeostasis. Furthermore, growing evidence suggests a correlation between EDCs exposure and tumorigenesis. Endoplasmic reticulum stress (ERS) has emerged as a vital cellular response to toxic stimuli, influencing apoptotic and proliferative pathways. Notably, ERS and autophagy are interconnected stress responses implicated in various pathological conditions. We propose that EDCs exert their toxic effects and facilitate disease progression by disrupting the ERS-autophagy signaling axis. This review critically examines the molecular interactions between ERS and autophagy induced by EDCs exposure, with the aim of advancing mechanistic understanding and identifying novel therapeutic targets for diseases associated with EDCs.