Oxidative stress damage as a detrimental factor in preterm birth pathology
Normal term and spontaneous preterm births (PTB) are documented to be associated with oxidative stress (OS), and imbalances in the redox system (balance between pro- and antioxidant) have been reported in the maternal-fetal intrauterine compartments. The exact mechanism of labor initiation either at...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2014-11-01
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| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fimmu.2014.00567/full |
| _version_ | 1811341169730256896 |
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| author | Ramkumar eMenon |
| author_facet | Ramkumar eMenon |
| author_sort | Ramkumar eMenon |
| collection | DOAJ |
| description | Normal term and spontaneous preterm births (PTB) are documented to be associated with oxidative stress (OS), and imbalances in the redox system (balance between pro- and antioxidant) have been reported in the maternal-fetal intrauterine compartments. The exact mechanism of labor initiation either at term or preterm by OS is still unclear, and this lack of understanding can partially be blamed for failure of antioxidant supplementation trials in PTB prevention. Based on recent findings from our laboratory, we postulate heterogeneity in host OS response. The physiologic (at term) and pathophysiologic (preterm) pathways of labor are not mediated by OS alone but by OS-induced damage to intrauterine tissues, especially fetal membranes of the placenta. OS damage affects all major cellular elements in the fetal cells, and this damage promotes fetal cell senescence (aging). The aging of the fetal cells are predominated by p38 mitogen activated kinase (p38MAPK) pathways. Senescing cells generate biomolecular signals that are uterotonic, triggering labor process. The aging of fetal cells is normal at term. However, aging is premature in PTB, especially in those PTBs complicated by preterm premature rupture of the membranes (pPROM), where elements of redox imbalances and OS damage are more dominant. We postulate that fetal cell senescence signals generated by OS damage are likely triggers for labor. This review highlights the mechanisms involved in senescence development at term and preterm by OS damage and provides insight into novel fetal signals of labor initiation pathways. |
| first_indexed | 2024-04-13T18:52:53Z |
| format | Article |
| id | doaj.art-793d8195f7bb47b7b7a13658cfdc28b3 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-04-13T18:52:53Z |
| publishDate | 2014-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-793d8195f7bb47b7b7a13658cfdc28b32022-12-22T02:34:21ZengFrontiers Media S.A.Frontiers in Immunology1664-32242014-11-01510.3389/fimmu.2014.00567116722Oxidative stress damage as a detrimental factor in preterm birth pathologyRamkumar eMenon0The University of Texas Medical BranchNormal term and spontaneous preterm births (PTB) are documented to be associated with oxidative stress (OS), and imbalances in the redox system (balance between pro- and antioxidant) have been reported in the maternal-fetal intrauterine compartments. The exact mechanism of labor initiation either at term or preterm by OS is still unclear, and this lack of understanding can partially be blamed for failure of antioxidant supplementation trials in PTB prevention. Based on recent findings from our laboratory, we postulate heterogeneity in host OS response. The physiologic (at term) and pathophysiologic (preterm) pathways of labor are not mediated by OS alone but by OS-induced damage to intrauterine tissues, especially fetal membranes of the placenta. OS damage affects all major cellular elements in the fetal cells, and this damage promotes fetal cell senescence (aging). The aging of the fetal cells are predominated by p38 mitogen activated kinase (p38MAPK) pathways. Senescing cells generate biomolecular signals that are uterotonic, triggering labor process. The aging of fetal cells is normal at term. However, aging is premature in PTB, especially in those PTBs complicated by preterm premature rupture of the membranes (pPROM), where elements of redox imbalances and OS damage are more dominant. We postulate that fetal cell senescence signals generated by OS damage are likely triggers for labor. This review highlights the mechanisms involved in senescence development at term and preterm by OS damage and provides insight into novel fetal signals of labor initiation pathways.http://journal.frontiersin.org/Journal/10.3389/fimmu.2014.00567/fullInflammationOxidative StresssenescenceOxidative damagePreterm BirthPremature rupture of fetal membranes |
| spellingShingle | Ramkumar eMenon Oxidative stress damage as a detrimental factor in preterm birth pathology Frontiers in Immunology Inflammation Oxidative Stress senescence Oxidative damage Preterm Birth Premature rupture of fetal membranes |
| title | Oxidative stress damage as a detrimental factor in preterm birth pathology |
| title_full | Oxidative stress damage as a detrimental factor in preterm birth pathology |
| title_fullStr | Oxidative stress damage as a detrimental factor in preterm birth pathology |
| title_full_unstemmed | Oxidative stress damage as a detrimental factor in preterm birth pathology |
| title_short | Oxidative stress damage as a detrimental factor in preterm birth pathology |
| title_sort | oxidative stress damage as a detrimental factor in preterm birth pathology |
| topic | Inflammation Oxidative Stress senescence Oxidative damage Preterm Birth Premature rupture of fetal membranes |
| url | http://journal.frontiersin.org/Journal/10.3389/fimmu.2014.00567/full |
| work_keys_str_mv | AT ramkumaremenon oxidativestressdamageasadetrimentalfactorinpretermbirthpathology |