Inflammaging and prognostic markers of endometriosis

In: Journal of obstetrics and women's diseases · 2024 · vol. 73(2) , pp. 129–136 · doi:10.17816/jowd622785 · W4399044210
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This review identifies molecular markers associated with inflammaging and their role in the pathogenesis and prognosis of endometriosis, drawing on a decade of literature.

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This 2024 narrative review examines how inflammaging, an age-associated inflammatory and cellular stress process driven by DNA damage, oxidative stress, mitochondrial dysfunction, and epigenetic changes, may contribute to the pathogenesis of endometriosis through senescence-associated secretory phenotype (SASP)-like alterations in endometrial cells. The authors systematized evidence from PubMed, Scopus, and Google Scholar over the prior decade to identify molecular mechanisms and candidate prognostic criteria, noting that there are currently no uniform diagnostic criteria or established molecular markers to predict endometriosis development or course. A key caveat is that the paper synthesizes published literature rather than presenting new experimental data, so conclusions depend on the heterogeneity and availability of prior studies. Relevance to endometriosis: the paper’s aim is specifically to identify molecular markers characterizing endometriosis during inflammaging, focusing on SASP and related inflammatory mechanisms tied to the condition.

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Abstract

Inflammaging, an age-associated inflammation, is a cellular stress response caused by DNA damage, activation of oncogenes or inactivation of tumor suppressors, oxidative stress, chemotherapy, mitochondrial dysfunction, or epigenetic changes. Damage to macromolecules leads to the cessation of proliferation due to the activation of pathways such as p53/p21CIP1 and p16INK4a/RB. These form the senescence-associated secretory phenotype (SASP), the molecular/cellular manifestations of which in endometrial cells have features similar to those observed in endometriosis. Presently, there are no uniform diagnostic criteria or established molecular markers that can predict the development and course of endometriosis. In this regard, it is relevant to develop new minimally invasive examination methods, statistically based criteria and molecular markers for early diagnosis and prognosis of endometriosis. This review article is devoted to identifying molecular markers that characterize the pathogenesis of endometriosis during inflaming. The aim of the study was to consider modern ideas about the mechanisms of inflaming and its role in the development of endometriosis to determine possible molecular markers for predicting the course of the pathology. We used the PubMed, Scopus and Google Scholar databases to analyze and systematize the literature over the past ten years. Our review reflects the main molecular mechanisms and prognostic criteria that characterize the development of endometriosis during inflaming.
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Inflammaging and prognostic markers of endometriosis - Authors: Shteiman A.A.1, Krylova Y.S.2,3, Dokhov M.A.3,4, Zubareva T.S.1,3 - Affiliations: - Saint Petersburg Institute of Bioregulation and Gerontology - Academician I.P. Pavlov First Saint Petersburg State Medical University - Saint Petersburg Institute of Phthisiopulmonology - Saint Petersburg State Pediatric Medical University - Issue: Vol 73, No 2 (2024) - Pages: 129-136 - Section: Reviews - Submitted: 01.11.2023 - Accepted: 22.02.2024 - Published: 27.05.2024 - URL: https://journals.eco-vector.com/jowd/article/view/622785 - DOI: https://doi.org/10.17816/JOWD622785 - ID: 622785 Cite item Abstract Inflammaging, an age-associated inflammation, is a cellular stress response caused by DNA damage, activation of oncogenes or inactivation of tumor suppressors, oxidative stress, chemotherapy, mitochondrial dysfunction, or epigenetic changes. Damage to macromolecules leads to the cessation of proliferation due to the activation of pathways such as p53/p21CIP1 and p16INK4a/RB. These form the senescence-associated secretory phenotype (SASP), the molecular/cellular manifestations of which in endometrial cells have features similar to those observed in endometriosis. Presently, there are no uniform diagnostic criteria or established molecular markers that can predict the development and course of endometriosis. In this regard, it is relevant to develop new minimally invasive examination methods, statistically based criteria and molecular markers for early diagnosis and prognosis of endometriosis. This review article is devoted to identifying molecular markers that characterize the pathogenesis of endometriosis during inflaming. The aim of the study was to consider modern ideas about the mechanisms of inflaming and its role in the development of endometriosis to determine possible molecular markers for predicting the course of the pathology. We used the PubMed, Scopus and Google Scholar databases to analyze and systematize the literature over the past ten years. Our review reflects the main molecular mechanisms and prognostic criteria that characterize the development of endometriosis during inflaming. Full Text About the authors Anastasia A. Shteiman Saint Petersburg Institute of Bioregulation and Gerontology Email: [email protected] ORCID iD: 0000-0002-4209-7133 SPIN-code: 4243-3599 MD, Cand. Sci. (Med.) Russian Federation, Saint PetersburgYulia S. Krylova Academician I.P. Pavlov First Saint Petersburg State Medical University; Saint Petersburg Institute of Phthisiopulmonology Email: [email protected] ORCID iD: 0000-0002-8698-7904 SPIN-code: 9729-7872 MD, Cand. Sci. (Med.) Russian Federation, Saint Petersburg; Saint PetersburgMikhail A. Dokhov Saint Petersburg Institute of Phthisiopulmonology; Saint Petersburg State Pediatric Medical University Author for correspondence. Email: [email protected] ORCID iD: 0000-0002-7834-5522 SPIN-code: 5849-5932 MD, Cand. Sci. (Med.) Russian Federation, 2-4 Ligovsky Ave., Saint Petersburg, 191036; Saint PetersburgTatyana S. Zubareva Saint Petersburg Institute of Bioregulation and Gerontology; Saint Petersburg Institute of Phthisiopulmonology Email: [email protected] ORCID iD: 0000-0001-9518-2916 SPIN-code: 2725-6105 Cand. Sci. (Biol.) Russian Federation, Saint Petersburg; 2-4 Ligovsky Ave., Saint Petersburg, 191036References - Secomandi L, Borghesan M, Velarde M, et al. The role of cellular senescence in female reproductive aging and the potential for senotherapeutic interventions. Hum Reprod Update. 2022;28(2):172–189. doi: 10.1093/humupd/dmab038 - Lean SC, Derricott H, Jones RL, et al. Advanced maternal age and adverse pregnancy outcomes: a systematic review and meta-analysis. PLoS One. 2017;12(10). doi: 10.1371/journal.pone.0186287 - Frederiksen LE, Ernst A, Brix N., et al. Risk of adverse pregnancy outcomes at advanced maternal age. Obstet Gynecol. 2018;131(3):457–463. doi: 10.1097/AOG.0000000000002504 - Pasquariello R, Ermisch AF, Silva E., et al. Alterations in oocyte mitochondrial number and function are related to spindle defects and occur with maternal aging in mice and humans. Biol Reprod. 2019;100(4):971–981. doi: 10.1093/biolre/ioy248 - Sultana Z, Maiti K, Dedman L, et al. Is there a role for placental senescence in the genesis of obstetric complications and fetal growth restriction? Am J Obstet Gynecol. 2018;218(2S):S762–S773. doi: 10.1016/j.ajog.2017.11.567 - Woods L, Perez-Garcia V, Kieckbusch J., et. al. Decidualisation and placentation defects are a major cause of age-related reproductive decline. Nat Commun. 2017;8(1):352. doi: 10.1038/s41467-017-00308-x - Daan NM, Fauser BC. Menopause prediction and potential implications. Maturitas. 2015;82(3):257–265. doi: 10.1016/j.maturitas.2015.07.019 - Chow ET, Mahalingaiah S. Cosmetics use and age at menopause: is there a connection? Fertil Steril. 2016;106(4):978–990. doi: 10.1016/j.fertnstert.2016.08.020 - Moslehi N, Mirmiran P, Tehrani FR, et al. Current evidence on associations of nutritional factors with ovarian reserve and timing of menopause: a systematic review. Adv Nutr. 2017;8(4):597–612. doi: 10.3945/an.116.014647 - Birch J, Gil J. Senescence and the SASP: many therapeutic avenues. Genes Dev. 2020;34(23–24):1565–1576. doi: 10.1101/gad.343129.120 - Gorgoulis V, Adams PD, Alimonti A., et. al. Cellular senescence: defining a path forward. Cell. 2019;179(4):813–827. doi: 10.1016/j.cell.2019.10.005 - McHugh D, Gil J. Senescence and aging: causes, consequences, and therapeutic avenues. J Cell Biol. 2018;217(1):65–77. doi: 10.1083/jcb.201708092. - Hoare M, Ito Y, Kang TW. Et NOTCH1 mediates a switch between two distinct secretomes during senescence. Nat Cell Biol. 2016;18(9):979–992. doi: 10.1038/ncb3397 - Chuprin A, Gal H, Biron-Shental T, et al. Cell fusion induced by ERVWE1 or measles virus causes cellular senescence. Genes Dev. 2013;27(21):2356–2366. doi: 10.1101/gad.227512.113. - Biran A, Zada L, Abou Karam P, et al. Quantitative identification of senescent cells in aging and disease. Aging Cell. 2017;16(4):661–671. doi: 10.1111/acel.12592 - Takasugi M, Okada R, Takahashi A, et al. Small extracellular vesicles secreted from senescent cells promote cancer cell proliferation through EphA2. Nat Commun. 2017;8:15729. doi: 10.1038/ncomms15728 - Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014;69(Suppl 1):S4–9. doi: 10.1093/gerona/glu057 - Vilas Boas L, Bezerra Sobrinho C, Rahal D, et al. Antinuclear antibodies in patients with endometriosis: a cross-sectional study in 94 patients. Hum Immunol. 2022;83(1):70–73. doi: 10.1016/j.humimm.2021.10.001 - Becker CM, Bokor A, Heikinheimo O, et al. ESHRE Endometriosis Guideline Group. ESHRE guideline: endometriosis. Hum Reprod Open. 2022;2022(2):1–26. doi: 10.1093/hropen/ hoac009 - Pomatto LCD, Davies KJA. Adaptive homeostasis and the free radical theory of ageing. Free Radic Biol Med. 2018;124:420–430. doi: 10.1016/j.freeradbiomed.2018.06.016 - Scutiero G, Iannone P, Bernardi G, et al. Oxidative stress and endometriosis: a systematic review of the literature. Oxid Med Cell Longev. 2017;2017. doi: 10.1155/2017/7265238 - Van Langendonckt A, Casanas-Roux F, Donnez J. Oxidative stress and peritoneal endometriosis. Fertil Steril. 2002;77(5):861–870. doi: 10.1016/s0015-0282(02)02959-x - Pertynska-Marczewska M, Diamanti-Kandarakis E. Aging ovary and the role for advanced glycation end products. Menopause. 2017;24(3):345–351. doi: 10.1097/GME.0000000000000755 - Merhi Z, Du XQ, Charron MJ. Postnatal weaning to different diets leads to different reproductive phenotypes in female offspring following perinatal exposure to high levels of dietary advanced glycation end products. F S Sci. 2022;3(1):95–105. doi: 10.1016/j.xfss.2021.12.001 - Young JM, McNeilly AS. Theca: the forgotten cell of the ovarian follicle. Reproduction. 2010;140(4):489–504. doi: 10.1530/REP-10-0094 - Laven JSE. Early menopause results from instead of causes premature general ageing. Reprod Biomed Online. 2022;45(3):421–424. doi: 10.1016/j.rbmo.2022.02.027 - Laven JSE. Genetics of menopause and primary ovarian insufficiency: time for a paradigm shift? Semin Reprod Med. 2020;38(4):256–262. doi: 10.1055/s-0040-1721796 - Ruth KS, Day FR, Hussain J, et al. Genetic insights into biological mechanisms governing human ovarian ageing. Nature. 2021; 596(7872):393–397. doi: 10.1038/s41586-021-03779-7 - Chico-Sordo L, Córdova-Oriz I, Polonio AM, et al. Reproductive aging and telomeres: are women and men equally affected? Mech Ageing Dev. 2021;198:111541. doi: 10.1016/j.mad.2021.111541 - Fernandes SG, Dsouza R, Khattar E. External environmental agents influence telomere length and telomerase activity by modulating internal cellular processes: implications in human aging. Environ Toxicol Pharmacol. 2021;85:103633. doi: 10.1016/j.etap.2021.103633 - Keefe DL. Telomeres and genomic instability during early development. Eur J Med Genet. 2020;63(2):103638. doi: 10.1016/j.ejmg.2019.03.002 - Kosebent EG, Uysal F, Ozturk S. The altered expression of telomerase components and telomere-linked proteins may associate with ovarian aging in mouse. Exp Gerontol. 2020;138:110975. doi: 10.1016/j.exger.2020.110975 - Sofiyeva N, Ekizoglu S, Gezer A, et al. Oral E. Does telomerase activity have an effect on infertility in patients with endometriosis? Eur J Obstet Gynecol Reprod Biol. 2017; 213:116–122. doi: 10.1016/j.ejogrb.2017.04.027 - Milewski Ł, Ścieżyńska A, Ponińska J, et al. Endometriosis is associated with functional polymorphism in the promoter of heme oxygenase 1 (HMOX1) gene. Cells. 2021;10(3):695. doi: 10.3390/cells10030695 - Agarwal SK, Chapron C, Giudice LC, et al. Clinical diagnosis of endometriosis: a call to action. Am J Obstet Gynecol. 2019;220(4):354.e1–354.e12. doi: 10.1016/j.ajog.2018.12.039 - Orazov MR, Radzinsky VE, Orekhov RE, et al. Endometriosis-associated infertility: pathogenesis and possibilities of hormone therapy in preparation for IVF. Gynecology, Obstetrics and Perinatology. 2022;21(2):90–98. EDN: BAVAIK doi: 10.20953/1726-1678-2022-2-90-98 - Anastasiu CV, Moga MA, Neculau EA, et al. Biomarkers for the noninvasive diagnosis of endometriosis: state of the artand future perspectives. Int J Mol Sci. 2020;21(5):1750. doi: 10.3390/ijms21051750 - Adamczyk M, Wender-Ozegowska E, Kedzia M. Epigenetic factors in eutopic endometrium in women with endometriosis and infertility. Int J Mol Sci. 2022;23(7):3804. doi: 10.3390/ijms23073804 - Laganà AS, Garzon S, Götte M, et al. The pathogenesis of endometriosis: molecular and cell biology insights. Int J Mol Sci. 2019;20(22):5615. doi: 10.3390/IJMS20225615 - Szukiewicz D, Stangret A, Ruiz-Ruiz C, et al. Estrogen- and progesterone (P4)-mediated epigenetic modifications of endometrial stromal cells (EnSCs) and/or mesenchymal stem/stromal cells (MSCs) in the etiopathogenesis of endometriosis. Stem Cell Rev Reports. 2021;17(4):1174–1193. doi: 10.1007/s12015-020-10115-5 - Amalinei C, Păvăleanu I, Lozneanu L, et al. Endometriosis — insights into a multifaceted entity. Folia Histochem Cytobiol. 2018;1(2):61–82. doi: 10.5603/FHC.a2018.0013 - Han SJ, Lee JE, Cho YJ, et al. Genomic function of estrogen receptor β in endometriosis. Endocrinology. 2019;160(11):2495–2516. doi: 10.1210/en.2019-00442 - McKinnon B, Mueller M, Montgomery G. progesterone resistance in endometriosis:an acquired property? Trends Endocrinol Metab. 2018;29(8):535–548. doi: 10.1016/j.tem.2018.05.006 - Perdaens O, van Pesch V. Molecular mechanisms of immunosenescene and inflammaging: relevance to the immunopathogenesis and treatment of multiple sclerosis. Front Neurol. 2021;12. doi: 10.3389/fneur.2021.811518 - Thomas V, Uppoor AS, Pralhad S, et al. Towards a common etiopathogenesis: periodontal disease and endometriosis. J Hum Reprod Sci. 2018;11:269–273. doi: 10.4103/jhrs.JHRS_8_18 - Fukui A, Mai C, Saeki S, et al. Pelvic endometriosis and natural killer cell immunity. Am J Reprod Immunol. 2021;85(4). doi: 10.1111/aji.13342 - Lagoumtzi SM, Chondrogianni N. Senolytics and senomorphics: natural and synthetic therapeutics in the treatment of aging and chronic diseases. Free Radic Biol Med. 2021;171:169–190. doi: 10.1016/j.freeradbiomed.2021.05.003 - Smolarz B, Szyłło K, Romanowicz H. Endometriosis: epidemiology, classification, pathogenesis, treatment and genetics (review of literature). Int J Mol Sci. 2021;22(19):10554. doi: 10.3390/ijms221910554317

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