Molecular links in endometriosis pathogenesis as targets for diagnosis and targeted therapy: a review

V. A. Yumasheva, Olga Lobanova, Н. Б. Парамонова, Daria D. Abasheva
In: Сибирский научный медицинский журнал · 2025 · vol. 45(4) , pp. 78–89 · doi:10.18699/ssmj20250408 · W4414033230
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review summarizes molecular factors in inflammation, neovascularization, invasion, autophagy, metabolism, and neurogenesis that may play roles in endometriosis pathogenesis and serve as targets for diagnosis and therapy.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text ⓘ

This paper is a literature review addressing the uncertain etiology and pathogenesis of endometriosis and highlighting diagnostic and targeted-therapy opportunities by synthesizing evidence on multiple biomolecular pathways. It compiles data implicating chronic inflammation mediators (including M2-associated factors, arginase-1, CD11b), angiogenesis/hypoxia signaling (VEGF, HIF-1α, decorin), invasion-related molecules (e.g., RPLP1, TWIST1, RON, CD47, TSP1, SIRPα), autophagy markers (LC3B-II, p62, Beclin, NLRC5), proliferative/metabolic activity (MCT, GLUT), and nerve fiber formation (NFASC, CHL1, c-Fos), while noting that existing theories do not fully explain causation and that the field still needs more effective diagnostic and therapeutic strategies. As an overarching caveat, it summarizes heterogeneous findings across studies rather than presenting new experimental results with uniform inclusion criteria or directly resolved mechanisms. This paper is centrally about endometriosis — it reviews molecular links in endometriosis pathogenesis to identify potential diagnostic markers and targeted therapy targets.

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Abstract

Endometriosis is a common gynecological disorder. Nowadays, its etiology and pathogenesis remain unknown. Its diagnosis and treatment are one of the most urgent problems. Existing theories do not fully explain the causes and mechanisms of the disease development, so the most effective treatment has not yet been found. Due to this fact, we cannot effectively prevent this disease. Many researchers try to solve this problem. The most important issue is studying various biomolecules' role in endometriosis development. In this review, we summarized data on some molecules that may play an important role in endometriosis development, including factors of chronic inflammation (M2-associated markers, arginase 1, CD11b), neovascularization (VEGF, HIF-1α, decorin), invasion (RPLP1, H3K27me3, TWIST1, RON, CD47, TSP1, SIRPα), autophagy (LC3B-II, p62, Beclin, NLRC5), proliferative activity and active metabolism in ectopic endometrial cells (MCT, GLUT), neurogenesis (NFASC, CHL1, c-Fos). The study of these molecules will help to deepen the understanding of the nature and mechanism of the disease, develop a diagnostic set of its markers, as well as effective treatment methods, including targeted therapy.
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Молекулярные звенья патогенеза эндометриоза – потенциальные мишени диагностики и таргетной терапии: обзор литературы https://doi.org/10.18699/SSMJ20250408 Аннотация Эндометриоз является одним из самых распространенных гинекологических заболеваний. Его этиология и патогенез на сегодняшний день не установлены. Актуальными проблемами также являются диагностика и лечение эндометриоза. Существующие теории не объясняют в полной мере причины возникновения и механизмы развития данного заболевания, что не позволяет разработать максимально эффективные тактики лечения и профилактики эндометриоза. Решению этих задач посвящено большое количество современных исследований, среди которых наиболее актуальным является изучение роли различных биомолекул в развитии эндометриоидной болезни. В данном обзоре мы обобщили современные данные по некоторым биомолекулам, которые могут играть важную роль в возникновении эндометриоза: факторам хронического воспаления (М2-ассоциированные факторы, аргиназа-1, CD11b), неоваскуляризации (VEGF, HIF-1α, декорин), инвазии (RPLP1, H3K27me3, TWIST1, RON, CD47, TSP1, SIRPα), аутофагии (LC3B-II, р62, Beclin, NLRC5), а также указывающим на выраженную пролиферативную активность, активный метаболизм в клетках эктопического эндометрия (MCT, GLUT) и формирование нервных волокон (NFASC, CHL1, c-Fos). Изучение данных молекул поможет углубить понимание природы и механизма развития заболевания, разработать диагностический набор его маркеров, а также эффективные методы лечения, в том числе таргетной терапии. Ключевые слова Об авторах В. А. ЮмашеваРоссия Юмашева Валентина Алексеевна 119991, г. Москва, ул. Трубецкая, 8, стр. 2 О. А. Лобанова Россия Лобанова Ольга Андреевна 119991, г. Москва, ул. Трубецкая, 8, стр. 2 Н. Б. 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