Peran Iron Overload Pada Proses Inflamasi Endometriosis

Cicilia Febriani Hayuningrum, Yordan Khaedir
In: Indonesian Journal of Health Science · 2022 · vol. 1(2) , pp. 51–56 · doi:10.54957/ijhs.v1i2.94 · W4206808746
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This review analyzes how iron overload contributes to endometriosis development by inducing inflammation and free radical molecule formation in the peritoneal cavity.

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This descriptive qualitative review analyzes literature on how iron overload contributes to the inflammatory and oxidative stress processes involved in endometriosis pathogenesis. It synthesizes evidence that iron overload can induce chronic inflammation and promote formation of free-radical molecules, thereby influencing the progression of endometriotic lesions. A major limitation is that the work is not original experimental research but a narrative literature review, so it does not present new data beyond what prior studies have reported. This paper is centrally about endometriosis — it specifically focuses on the role of iron overload in driving chronic inflammation and oxidative stress in endometriosis.

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Abstract

Endometriosis merupakan kondisi ginekologikal yang ditandai dengan adanya implantasi jaringan endometrium di luar rongga uterus. Endometriosis ditandai dengan terjadinya proses inflamasi kronik di dalam rongga peritoneal, yang menimbulkan berbagai gejala pada penderitanya. Banyak faktor terlibat dalam proses inflamasi kronik endometriosis, salah satunya adalah stres oksidatif. Stres oksidatif pada rongga peritoneal wanita dengan endometriosis salah satunya terkait dengan kondisi iron overload. Hasil artikel review ini menunjukkan bahwa iron overload merupakan salah satu faktor yang berperan dalam perjalanan dan perkembangan lesi endometriosis melalui kemampuannya menginduksi proses inflamasi dan pembentukan molekul radikal bebas. Tujuan artikel review berikut adalah untuk menganalisis dan mengetahui bagaimana peranan iron overload dalam perjalanan penyakit endometriosis, sehingga harapannya dapat menjadi salah satu target pengobatan endometriosis. Metode penelitian yang digunakan yaitu deskriptif kualitatif dengan pengambilan materi berbasis literatur.
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Peran Iron Overload Pada Proses Inflamasi Endometriosis DOI: https://doi.org/10.54957/ijhs.v1i2.94Kata Kunci: endometriosis, inflamasi kronik, stress oksifdatif, iron overloadAbstrak Endometriosis merupakan kondisi ginekologikal yang ditandai dengan adanya implantasi jaringan endometrium di luar rongga uterus. Endometriosis ditandai dengan terjadinya proses inflamasi kronik di dalam rongga peritoneal, yang menimbulkan berbagai gejala pada penderitanya. Banyak faktor terlibat dalam proses inflamasi kronik endometriosis, salah satunya adalah stres oksidatif. Stres oksidatif pada rongga peritoneal wanita dengan endometriosis salah satunya terkait dengan kondisi iron overload. Hasil artikel review ini menunjukkan bahwa iron overload merupakan salah satu faktor yang berperan dalam perjalanan dan perkembangan lesi endometriosis melalui kemampuannya menginduksi proses inflamasi dan pembentukan molekul radikal bebas. Tujuan artikel review berikut adalah untuk menganalisis dan mengetahui bagaimana peranan iron overload dalam perjalanan penyakit endometriosis, sehingga harapannya dapat menjadi salah satu target pengobatan endometriosis. Metode penelitian yang digunakan yaitu deskriptif kualitatif dengan pengambilan materi berbasis literatur. Referensi Baranov, V., Malysheva, O., Yarmonlinskaya, M., (2018). Pathogenomics of endometriosis development. Int J Mol Sci. 19:1–11. Barragan, F., Irwin, J.C., Balayan, S., Erikson, D., (2016). Human endometrial fibroblasts derived from mesenchymal progenitors inherit progesterone resistance and acquire an inflammatory phenotype in the endometrial niche in endometriosis. Biol Reprod. 94, 1–20. Burney, R.O., and Giudice, L., (2012). Pathogenesis and pathophysiology of endometriosis. NIH Public Access. 98(3). Defere, S., Ramos, G. R., Louses, J., Colette, S., Donnez, O; Donnez, J, Langendonckt, A. (2011). Insight into iron and nuclear factor kappa B involvement in chronic inflammatory processes in peritoneal enometriosis. Histol Histopathol. 26,1083–1092. Donnez, J., Binda, M., Donnez, O., Dolmans M-M. (2016). Oxidative Stress in The Pelvic Cavity and Its Role In The Pathogenesis of Endometriosis. Elsevier. 106,1011–1016. Eisenberg, VH., Weil, C., Chodick, G., Shalev V. (2017). Epidemiology of endometriosis: a large population-based database study from a healthcare provider with 2 million members. BJOG. Giliney, Me., Oral, B., Karahan, N., Mungan, T. (2008). Regression of Endometrial Explants in A Rat Model of Endometriosis Treated with Melatonin. Elsevier. 89,934–941. Morgan, M., and Liu Z., (2011). Crosstalk of reactive oxygen species and NF-ĸB signaling. Nature. 21,103–115. Oeckinghaus, A., and Ghosh, S., (2009). The NF-ĸB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol. Parasar, P., Ozcan, P., Terry K. Endometriosis: epidemiology, diagnosis and clinical management. Curr Obs Gynecol Rep. 6,34–41. Ramos, G. R., and Defere, S. D. L., (2019). Nuclear factor-kappaB: a main regulator of inflammation and cell survival in endometriosis pathophysiology. Elsevier. 98(3), 520–525. Rocha, A.L., Reis, M.F.., Taylor, R., (2013). Angiogenesis and endometriosis. Obstet Gynecol Int Rutherford, E., Hill, A., Hopkins, A., (2018). Adhesion in physiological, benign and malignant proliferative states of the endometrium: microenvironment and the clinical big picture. Cells. 7(43). Seli, E., Berkkanoglu, M., Arici, A., (2003). Pathogenesis of endometriosis. Elsevier. 30, 41–61. Sourial, S., and Tempest, N.H.D., (2014). Theories on the pathogenesis of endometriosis. Hindawi. Szczepariska, M., Kozlik, J., Skrzypczak, J., Mikolajczyk M. (2003). Oxidative Stress May Be A Piece In The Endometriosis Puzzle. Elsevier. 79,1288–1293. Wu, J., Xie, H., Yao, S., Liang, Y., (2017). Macrophage and nerve interaction in endometriosis. J Neuroinflammation. 14(53). Yavuz, S., Aydin, N., Celik, O., Yilmaz, E., Ozerol, E., Tanbek K. (2014). Resveratrol Successfully Treats Experimental Endometriosis Through Modulation of Oxidative Stress and Lipid Peroxidation. J Cancer Res Ther. 10(2),324–329. Unduhan Diterbitkan Cara Mengutip Terbitan Bagian Lisensi Hak Cipta (c) 2021 Indonesian Journal of Health Science Artikel ini berlisensi Creative Commons Attribution 4.0 International License.

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