TY - JOUR
T1 - Unraveling the role of lncRNA in Endometriosis-Associated immune system Dysregulation
T2 - Exploring the intricate immunological changes and disrupted signaling pathways
AU - Oghenemaro, Enwa Felix
AU - Hjazi, Ahmed
AU - Altalbawy, Farag M.A.
AU - Kyada, Ashishkumar
AU - Nathiya, Deepak
AU - Kaur, Parjinder
AU - Uthirapathy, Subasini
AU - Kariem, Muthena
AU - Kumar, M. Ravi
AU - Naser, Israa Habeeb
N1 - Publisher Copyright:
© 2025 American Society for Histocompatibility and Immunogenetics
PY - 2025/3
Y1 - 2025/3
N2 - A chronic illness known as endometriosis impacts women who are of reproductive maturity. It may be a factor in fertility problems, breast or ovarian cancer, asthma, cardiovascular illness, or pelvic pain. Studies have indicated that malfunctioning of the immune system is one of the prerequisites for the occurrence of endometrial diseases. Immune cells such as neutrophils and macrophages seem to be involved in the angiogenesis, proliferation, and invasion of endometriosis cells in a particular way. In this regard, defensive substances and cytokines secreted by immune cells impact the endometriosis milieu. Long non-coding RNAs (lncRNAs) mediate gene expression throughout the inflammatory process. According to the current studies, dysfunctional lncRNAs have been linked to several human disorders, including endometriosis. These non-coding RNAs are essential for immunological mechanisms because they regulate interactions between proteins or the capability of RNA and DNA to assemble, which plays a role in differentiation, cell migration, and the synthesis of inflammatory cytokines. Due to the brilliant role of lncRNAs in immune responses and the undeniable role of the immune system in reproduction biology, this study aimed to review the role of deregulated lncRNAs in immune system disorders and its mutual effect on endometriosis formation and development. Further study should identify the significance of lncRNAs linked to the disease via in-vitro and animal model investigations and the importance of uncharacterized lncRNAs found by endometriosis transcriptome studies.
AB - A chronic illness known as endometriosis impacts women who are of reproductive maturity. It may be a factor in fertility problems, breast or ovarian cancer, asthma, cardiovascular illness, or pelvic pain. Studies have indicated that malfunctioning of the immune system is one of the prerequisites for the occurrence of endometrial diseases. Immune cells such as neutrophils and macrophages seem to be involved in the angiogenesis, proliferation, and invasion of endometriosis cells in a particular way. In this regard, defensive substances and cytokines secreted by immune cells impact the endometriosis milieu. Long non-coding RNAs (lncRNAs) mediate gene expression throughout the inflammatory process. According to the current studies, dysfunctional lncRNAs have been linked to several human disorders, including endometriosis. These non-coding RNAs are essential for immunological mechanisms because they regulate interactions between proteins or the capability of RNA and DNA to assemble, which plays a role in differentiation, cell migration, and the synthesis of inflammatory cytokines. Due to the brilliant role of lncRNAs in immune responses and the undeniable role of the immune system in reproduction biology, this study aimed to review the role of deregulated lncRNAs in immune system disorders and its mutual effect on endometriosis formation and development. Further study should identify the significance of lncRNAs linked to the disease via in-vitro and animal model investigations and the importance of uncharacterized lncRNAs found by endometriosis transcriptome studies.
KW - Cytokines
KW - Endometriosis
KW - Immune system regulation
KW - Inflammation
KW - lncRNAs
UR - http://www.scopus.com/inward/record.url?scp=85216887483&partnerID=8YFLogxK
U2 - 10.1016/j.humimm.2025.111248
DO - 10.1016/j.humimm.2025.111248
M3 - Review article
C2 - 39913955
AN - SCOPUS:85216887483
SN - 0198-8859
VL - 86
JO - Human Immunology
JF - Human Immunology
IS - 2
M1 - 111248
ER -