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Inflammation and Resolution in Endometriosis: From Science to Clinic
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Inflammation and Resolution in Endometriosis: From Science to Clinic

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 14832

Special Issue Editor

Dr. Pedro-Antonio Regidor

E-Mail Website
Guest Editor
Exeltis Healthcare, Adalperostr, 84, 85737 Ismaning, Germany
Interests: endometriosis; laparoscopic surgery; gynaecological surgery; reproductive medicine

Special Issue Information

Dear colleagues,

Endometriosis is a hormonal dependant benign disease that affects up to 12% of women during reproductive life. In the past decade, the number of patients with endometriosis has continued to increase and its aetiology has not been clearly elucidated. It is considered a chronic inflammatory and proliferative disease whose onset and development involves immunologic mechanisms.

Basic science research has also described the inflammation associated with the disease and its correlation to dysmenorrhoea and chronic pelvic pain.

A local burst of prostaglandins induced by macrophages and mesothelial cells surrounding the endometriotic implants are involved in the process of chronic pain.

Describing the molecular mechanisms of inflammation and resolution of inflammation in endometriosis lesions will improve the ability to develop targeted pain reducing substances.

The special issue focuses on the molecular description of inflammatory and pro resolving molecular aspects and their possible implications in the management of the endometriosis associated pain.

Dr. Pedro-Antonio Regidor
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • endometriosis
  • chronic pain
  • inflammation
  • resolution of inflammation

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Published Papers (3 papers)

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Research

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16 pages, 2636 KiB  
Article
Overexpression of Human Estrogen Biosynthetic Enzyme Hydroxysteroid (17beta) Dehydrogenase Type 1 Induces Adenomyosis-like Phenotype in Transgenic Mice
by Taija Heinosalo, Kalle T. Rytkönen, Niina Saarinen, Päivi Järvensivu, Pauliina Damdimopoulou, Leena Strauss, Satu Orasniemi, Petricia Horshauge, Michael Gabriel, Pasi Koskimies, Claes Ohlsson, Pauliina Kronqvist and Matti Poutanen
Int. J. Mol. Sci. 2022, 23(9), 4815; https://doi.org/10.3390/ijms23094815 - 27 Apr 2022
Cited by 5 | Viewed by 2491
Abstract
Hydroxysteroid (17beta) dehydrogenase type 1 (HSD17B1) is an enzyme that converts estrone to estradiol, while adenomyosis is an estrogen-dependent disease with poorly understood pathophysiology. In the present study, we show that mice universally over-expressing human estrogen biosynthetic enzyme HSD17B1 (HSD17B1TG mice) present with [...] Read more.
Hydroxysteroid (17beta) dehydrogenase type 1 (HSD17B1) is an enzyme that converts estrone to estradiol, while adenomyosis is an estrogen-dependent disease with poorly understood pathophysiology. In the present study, we show that mice universally over-expressing human estrogen biosynthetic enzyme HSD17B1 (HSD17B1TG mice) present with adenomyosis phenotype, characterized by histological and molecular evaluation. The first adenomyotic changes with endometrial glands partially or fully infiltrated into the myometrium appeared at the age of 5.5 months in HSD17B1TG females and became more prominent with increasing age. Preceding the phenotype, increased myometrial smooth muscle actin positivity and increased amount of glandular myofibroblast cells were observed in HSD17B1TG uteri. This was accompanied by transcriptomic upregulation of inflammatory and estrogen signaling pathways. Further, the genes upregulated in the HSD17B1TG uterus were enriched with genes previously observed to be induced in the human adenomyotic uterus, including several genes of the NFKB pathway. A 6-week-long HSD17B1 inhibitor treatment reduced the occurrence of the adenomyotic changes by 5-fold, whereas no effect was observed in the vehicle-treated HSD17B1TG mice, suggesting that estrogen is the main upstream regulator of adenomyosis-induced uterine signaling pathways. HSD17B1 is considered as a promising drug target to inhibit estrogen-dependent growth of endometrial disorders. The present data indicate that HSD17B1 over-expression in TG mice results in adenomyotic changes reversed by HSD17B1 inhibitor treatment and HSD17B1 is, thus, a potential novel drug target for adenomyosis. Full article
(This article belongs to the Special Issue Inflammation and Resolution in Endometriosis: From Science to Clinic)
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14 pages, 3763 KiB  
Article
Regulation of Inflammatory and Proliferative Pathways by Fotemustine and Dexamethasone in Endometriosis
by Tiziana Genovese, Rosalba Siracusa, Ramona D’Amico, Marika Cordaro, Alessio Filippo Peritore, Enrico Gugliandolo, Rosalia Crupi, Angela Trovato Salinaro, Emanuela Raffone, Daniela Impellizzeri, Salvatore Cuzzocrea, Roberta Fusco and Rosanna Di Paola
Int. J. Mol. Sci. 2021, 22(11), 5998; https://doi.org/10.3390/ijms22115998 - 1 Jun 2021
Cited by 7 | Viewed by 3200
Abstract
Endometriosis is a common disease. Its pathogenesis still remains uncertain, but it is clear that cell proliferation, apoptosis and chronic inflammation play an important role in its development. This paper aimed to investigate the anti-proliferative and anti-inflammatory effects of a combined therapy with [...] Read more.
Endometriosis is a common disease. Its pathogenesis still remains uncertain, but it is clear that cell proliferation, apoptosis and chronic inflammation play an important role in its development. This paper aimed to investigate the anti-proliferative and anti-inflammatory effects of a combined therapy with fotemustine and dexamethasone. Endometriosis was induced by intraperitoneal injections of uterine fragments from donor animals to recipient animals. Next, the pathology was allowed to develop for 7 days. On the seventh day, fotemustine was administered once and dexamethasone was administered daily for the next 7 days. On Day 14, the animals were sacrificed, and peritoneal fluids and lesions were explanted. In order to evaluate the gastrointestinal side effects of the drugs, stomachs were harvested as well. The combined therapy of fotemustine and dexamethasone reduced the proinflammatory mediator levels in the peritoneal fluid and reduced the lesions’ area and diameter. In particular, fotemustine and dexamethasone administration reduced the heterogeneous development of endometrial stroma and glands (histological analysis of lesions) and hyperproliferation of endometriotic cells (immunohistochemical analysis of Ki67 and Western blot analysis of PCNA) through the mitogen-activated protein kinase (MAPK) signaling pathway. Combined fotemustine and dexamethasone therapy showed anti-inflammatory effects by inducing the synthesis of anti-inflammatory mediators at the transcriptional and post-transcriptional levels (Western blot analysis of NFκB, COX-2 and PGE2 expression). Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance. Full article
(This article belongs to the Special Issue Inflammation and Resolution in Endometriosis: From Science to Clinic)
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Review

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19 pages, 1240 KiB  
Review
The Role of Peritoneal Macrophages in Endometriosis
by Tamara N. Ramírez-Pavez, María Martínez-Esparza, Antonio J. Ruiz-Alcaraz, Pilar Marín-Sánchez, Francisco Machado-Linde and Pilar García-Peñarrubia
Int. J. Mol. Sci. 2021, 22(19), 10792; https://doi.org/10.3390/ijms221910792 - 6 Oct 2021
Cited by 45 | Viewed by 8010
Abstract
Endometriosis is an estrogen-dependent gynecological disorder, defined as the growth of endometrial stromal cells and glands at extrauterine sites. Endometriotic lesions are more frequently located into the abdominal cavity, although they can also be implanted in distant places. Among its etiological factors, the [...] Read more.
Endometriosis is an estrogen-dependent gynecological disorder, defined as the growth of endometrial stromal cells and glands at extrauterine sites. Endometriotic lesions are more frequently located into the abdominal cavity, although they can also be implanted in distant places. Among its etiological factors, the presence of immune dysregulation occupies a prominent place, pointing out the beneficial and harmful outcomes of macrophages in the pathogenesis of this disease. Macrophages are tissue-resident cells that connect innate and adaptive immunity, playing a key role in maintaining local homeostasis in healthy conditions and being critical in the development and sustainment of many inflammatory diseases. Macrophages accumulate in the peritoneal cavity of women with endometriosis, but their ability to clear migrated endometrial fragments seems to be inefficient. Hence, the characteristics of the peritoneal immune system in endometriosis must be further studied to facilitate the search for new diagnostic and therapeutic tools. In this review, we summarize recent relevant advances obtained in both mouse, as the main animal model used to study endometriosis, and human, focusing on peritoneal macrophages obtained from endometriotic patients and healthy donors, under the perspective of its future clinical translation to the role that these cells play on this pathology. Full article
(This article belongs to the Special Issue Inflammation and Resolution in Endometriosis: From Science to Clinic)
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