ArticleBiomedicines2022
Leptin Stimulates Endometriosis Development in Mouse Models.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Unraveling the genetic links between stature and disease in East Asians: A multi-biobank genetic correlation and risk prediction study.PLoS genetics · 2026Article
- Review
- Association between body mass index and anti-Müllerian hormone in women with ovarian endometrioma and dermoid cyst.Frontiers in endocrinology · 2026Article
- The interplay between endometriosis and obesity.Trends in endocrinology and metabolism: TEM · 2025Review
- Noninvasive Detection and Thermal Ablation Therapy of Endometriosis Using Silica-Coated Gold Nanorods.Advanced nanobiomed research · 2025Article
- The development of a preclinical swine model for endometriosis†.Biology of reproduction · 2025Article
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
- FOXA2 loss results in an increase of endometriosis development and LIF reveals a therapeutic effect for endometriosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Interplay of Uterine Health and Obesity: A Comprehensive Review.Biomedicines · 2024Review
- The kisspeptin system in and beyond reproduction: exploring intricate pathways and potential links between endometriosis and polycystic ovary syndrome.Reviews in endocrine & metabolic disorders · 2024Review
- High-fat diets promote peritoneal inflammation and augment endometriosis-associated abdominal hyperalgesia.Frontiers in endocrinology · 2024Article
- Transgenic mice applications in the study of endometriosis pathogenesis.Frontiers in cell and developmental biology · 2024Review
- High-fat diets promote peritoneal inflammation and augment endometriosis-associated abdominal hyperalgesia.bioRxiv : the preprint server for biology · 2023Article
- A Pilot Study on the Co-existence of Diabetes and Endometriosis in Reproductive-Age Women: Potential for Endometriosis Progression.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Endometriosis is a chronic inflammatory condition in women, and obesity leads to an inflammatory condition that is directly involved in the etiology of endometriosis. However, observational studies have shown an inverse correlation between endometriosis and a low body mass index (BMI). Obesity does not protect against endometriosis, and on the contrary, an increased BMI may lead to more severe forms of the disease. To determine the effect of obesity on endometriosis, diet-induced and genetically engineered obese mouse models were integrated with endometriosis mouse models with fluorescence-tagged ectopic lesions. High-fat diet-induced obese mice revealed a significant increase in endometriosis development compared with regular-diet control mice. However, obese recipient mice with leptin deficiency and leptin receptor deficiency showed suppressed endometriosis development compared with control mice. Furthermore, donor uterine tissues with leptin deficiency and leptin receptor deficiency suppressed endometriosis development compared with control donor in control recipient mice. Importantly, we revealed that aberrant high levels of leptin concentration significantly increased endometriosis development compared with vehicle treatment group in control mice with normal body weight. Our results suggest that leptin and its receptor are critical for endometriosis development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.