Adenomyosis (AM) has become a prevalent and challenging disease due to the constant rise in its incidence rate over recent years [1]. Clinical manifestations of AM include increased menstrual bleeding, advancing dysmenorrhea, and even infertility, adversely affecting patients' overall lives and daily work [2]. Hence, conducting a thorough investigation into the development and progression of AM is imperative.

Despite being a benign condition, AM exhibits a malignant proliferative potential similar to tumors. Its histological manifestation involves the invasion of endometrial stromal and glandular epithelial cells into the myometrium of the uterus [3,4]. According to current research, abnormal proliferative potential in AM development results from several factors acting in concert, such as estrogen imbalance, hypoxic injury, chronic pro-inflammatory status, and others [5,6]. However, the intricate interplay between these factors contributing to the pathogenesis of AM is yet to be fully understood.

Research has verified that endometrial hypoxia is a crucial instigating mechanism in AM [7]. Mitochondria, being highly responsive sensors to hypoxia, can play a part in the intercommunication between hypoxic damage and the aberrant proliferative potential. Our previous findings have confirmed that hypoxic mitochondria in AM endometrial cells undergo structural and functional impairments, which can lead to the excessive activation of mitophagy [8]. Recent research suggests that the upregulation of mitophagy can potentially result in the release of mitochondrial DNA (mtDNA) into the cytoplasm [9]. This process can activate the cGAS-STING signaling pathway, thereby promoting the development of a chronic pro-inflammatory state through the enhancement of type I interferon-mediated autoimmune response [10]. It has been demonstrated that the cGAS-STING signaling pathway activated by mtDNA plays a critical role in the abnormal proliferation ability of tumors [11]. Although AM exhibits specific tumor-like characteristics and is closely associated with chronic pro-inflammatory conditions [12], the particular role of the cGAS-STING signaling pathway, activated by mtDNA, in the occurrence and development of AM remains uncertain.

Therefore, the objective of this study is to observe the alterations in the levels of the cGAS-STING signaling pathway, activated by mtDNA, in individuals diagnosed with AM and in vitro endometrial stromal cells (ESCs). Moreover, the study aims to establish a correlation between this pathway and the abnormal invasive capability of cells, thus offering novel insights into the underlying mechanisms contributing to the development of AM.