Immune Dysregulation in Endometriomas: Implications for Inflammation.
Izabela Dymanowska-DyjakBarbara TerpiłowskaIzabela Morawska-MichalskaAdam MichalskiGrzegorz PolakMichał TerpiłowskiMansur Rahnama-HezavahEwelina GrywalskaPublished in: International journal of molecular sciences (2024)
The most common manifestation of endometriosis, a condition characterized by the presence of endometrial-like tissue outside of the uterus, is the endometrioma, a cystic ovarian lesion. It is a commonly occurring condition associated with chronic pelvic pain exacerbated prior to and during menstruation, as well as infertility. The exact pathomechanisms of the endometrioma are still not fully understood. Emerging evidence suggests a pivotal role of immune dysregulation in the pathogenesis of endometriomas, primarily influencing both local and systemic inflammatory processes. Among the factors implicated in the creation of the inflammatory milieu associated with endometriomas, alterations in both serum and local levels of several cytokines stand out, including IL-6, IL-8, and IL-1β, along with abnormalities in the innate immune system. While numerous signaling pathways have been suggested to play a role in the inflammatory process linked to endometriomas, only NF-κB has been conclusively demonstrated to be involved. Additionally, increased oxidative stress, both resulting from and contributing to endometriomas, has been identified as a primary driver of both systemic and local inflammation associated with the condition. This article reviews the current understanding of immune dysfunctions in the endometrioma and their implications for inflammation.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- ischemia reperfusion injury
- dna damage
- signaling pathway
- immune response
- chronic pain
- pi k akt
- randomized controlled trial
- metabolic syndrome
- pain management
- rectal cancer
- type diabetes
- epithelial mesenchymal transition
- endometrial cancer
- spinal cord injury
- spinal cord
- neuropathic pain
- toll like receptor
- drug induced
- nuclear factor
- inflammatory response
- adipose tissue
- meta analyses