Background and Objectives: The pathogenesis of placenta accreta spectrum disorder (PASD) is influenced by the inflammatory process. Therefore, the examination of biomarkers related to the inflammatory process, namely matrix metalloproteinase (MMP) and CXC motif chemokine receptor 2 (CXCR2), is expected to bring researchers to a bright spot regarding the pathogenesis of PASD. This study analyzes the role of CXCR2, MMP-2, and MMP-9 in the pathogenesis of PASD. Materials and Methods: An observational study with a case–control design was conducted to assess differences in the mean density of CXCR2, MMP-2, and MMP-9 immunostaining in placental and uterine tissue in 17 patients with PASD and 34 patients without PASD at the Department of Obstetrics and Gynecology, Dr. Mohammad Hoesin Hospital Palembang. The expression of CXCR2, MMP-2, and MMP-9 was measured by immunohistochemistry analysis. The data were analyzed using STATA version 15. Results: There were no significant differences in the mean levels of MMP-2 expression in patients with and without PASD. There were significant differences in the expression of placental CXCR2 (p = 0.003), uterine CXCR2 (p < 0.001), and uterine MMP-9 (p = 0.018) in patients with and without PASD. Conclusions: CXCR2 and MMP-9 may play a role in the pathogenesis of PASD.

Background and Objectives: Preeclampsia has been linked to an inflammatory response that may be brought on by endothelial cell dysfunction. This paper investigates the pathomechanism of syncytiotrophoblast basement membrane (STBM) damage and Placental Protein 13 (PP13) release, which may have a role in systemic endothelial dysfunction in preeclampsia. Materials and Methods: This comparative cross-sectional study involves 54 preeclampsia patients (27 early-onset preeclampsia and 27 late-onset preeclampsia) and 27 pregnant women with normal blood pressure. An enzyme-linked immunosorbent assay was performed to evaluate maternal blood levels of PP13. Following birth, a portion of the placenta was collected for transmission electron microscope (TEM) and immunohistochemical (IHC) analysis. The data were analyzed using STATA version 15. Results: PP13 expression in the placental syncytiotrophoblast was significantly lower in the early-onset preeclampsia, compared to late-onset preeclampsia and normotensive pregnancy, group (p < 0.001). In contrast, serum PP13 levels were found to be the highest in the early-onset preeclampsia group, although no significant difference were found in mean maternal serum levels of PP13 between the three groups. The decreased PP13 expression in placental syncytiotrophoblast can be attributed to the greater extent of damage in the STBM in early-onset preeclampsia that leads to the release of a larger amount of PP13 into maternal circulation. The hypothesis aligns with the TEM analysis results. Preeclamptic pregnancies showed placental syncytiotrophoblast aponeurosis, whereas normotensive pregnancies did not. Placental lesions and STBM shedding were found to be more pronounced in early-onset preeclampsia compared to late-onset preeclampsia. Conclusions: PP13 and STBM damage may play a role in systemic endothelial dysfunction in preeclampsia.

BACKGROUND Women with endometriosis experience significantly reduced fertility, potentially linked to mitochondrial dysfunction. This study investigates the impact of endometriosis on oocyte mitochondrial morphology and cardiolipin levels, key indicators of mitochondrial health and function. MATERIAL AND METHODS Thirty-two healthy mice were randomly allocated into 2 groups: a control group (P0, n=16) and an endometriosis model group (P1, n=16). Endometriosis was induced via intraperitoneal injection of endometrial tissue, and oocytes were retrieved following superovulation. Mitochondrial morphology was analyzed using transmission electron microscopy, and cardiolipin levels were measured via ELISA. Statistical analyses included the Fisher exact test, Mann-Whitney U test, and Spearman correlation. RESULTS Mitochondrial morphology in oocytes from the endometriosis group exhibited significant structural abnormalities, compared with controls (P<0.001). Class III and IV mitochondria, characterized by disrupted membranes and cristae, were predominantly observed in the endometriosis group. Cardiolipin levels were significantly reduced in the endometriosis group, compared with controls (P<0.001). A positive correlation (r=0.73, P<0.001) was identified between mitochondrial morphological changes and cardiolipin levels, indicating that structural mitochondrial damage was strongly associated with reduced cardiolipin levels. CONCLUSIONS Endometriosis induces significant mitochondrial abnormalities and decreases cardiolipin levels in oocytes, suggesting mitochondrial dysfunction as a critical factor in reduced fertility. These findings underscore the potential of targeting mitochondrial health to improve reproductive outcomes in women with endometriosis.

The recent increase in placenta accreta spectrum has been correlated with a rise in the rate of cesarean sections. A recent study provides evidence that hampered wound healing results in cesarean scar defects that lead to a failure in the normal process of decidualization and deeper adherence of trophoblasts. Matrix metalloproteinase (MMP) is crucial in every step of wound healing as it alters the wound matrix, facilitating cell migration, as well as tissue remodeling. MMP-9 expression is higher in placental and decidual tissue in cases of placenta accreta. Based on these findings, assessment of MMP-9 expression can shed new light on the etiopathology of placenta accreta spectrum disorder and can be a potential diagnostic marker.

Artificial intelligence (AI) and regenerative medicine are becoming inextricably linked. As a result, the long-term outlook for the advancement of AI, regenerative medicine, and stem cells in the healthcare industry is incredibly bright. AI is being used in healthcare to discover new drugs and to provide personalized medicine based on big data. It can improve medical diagnosis and treatment plans. Regenerative medicine has the potential to repair damaged tissues and organs through stem cell-based regenerative medicine. Stem cell research is also undergoing significant development as a major component of the approach to regenerative medicine. In the future, it is expected that it will contribute to more personalized and more effective treatments. Integrating AI can help model and simulate cellular behavior, analyze, and process images for cell tracking and tissue engineering, and analyze large amounts of genomic and proteomic data. Together, these fields have the potential to transform healthcare and improve patient outcomes.