Inflammation-metabolism-fibrosis axis: mechanisms and therapeutic strategies targeting the chronicity of pelvic inflammatory disease.

Pelvic inflammatory disease (PID) is a common infectious disease in gynecology; it can easily develop into chronic inflammation and tissue fibrosis. These conditions severely affect patients' reproductive health and quality of life. In recent years, studies have found that the inflammatory response, metabolic reprogramming, and fibrotic process interact through complex molecular mechanisms, forming an inflammation-metabolism-fibrosis axis. This axis has become a core driving factor in the chronic progression of PID. Specifically, this axis involves dynamic adjustments of immune cell metabolism, mitochondrial dysfunction, and activation of fibroblasts. These changes collectively promote the persistent presence of tissue damage and fibrosis development. Although some related signaling pathways and intercellular interactions have been revealed in previous studies, the overall regulatory mechanism underlying this network is still not fully understood. This limitation hinders the development of precise treatment strategies. This article systematically summarizes the key role of the inflammation-metabolism-fibrosis axis in the chronic progression of PID, analyzes the relationship between relevant molecular mechanisms and their clinical manifestations, and focuses on potential therapeutic targets and strategies based on this axis. By integrating the latest research findings, this article aims to provide theoretical support for elucidating the pathological mechanisms of PID and clinical interventions, thereby promoting the development of precision medicine.