ArticleFrontiers in pharmacology2020
NLRC5 Inhibits Inflammation of Secretory Phase Ectopic Endometrial Stromal Cells by Up-Regulating Autophagy in Ovarian Endometriosis.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Parthenolide attenuated the endometriosis-like lesions by activating autophagy and suppressing NLRP3 inflammasome activity.Iranian journal of basic medical sciences · 2026Article
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
- Unveiling the Role of PNMA2 in Endometriosis: From Proliferation and Apoptosis to Immunomodulation.Journal of cellular and molecular medicine · 2025Article
- Targeting NLRC5 in cardiomyocytes protects postinfarction cardiac injury by enhancing autophagy flux through the CAVIN1/CAV1 axis.Communications biology · 2025Article
- Autophagy Involvement in Non-Neoplastic and Neoplastic Endometrial Pathology: The State of the Art with a Focus on Carcinoma.International journal of molecular sciences · 2024Review
- NLRC5 exerts anti-endometriosis effects through inhibiting ERβ-mediated inflammatory response.BMC medicine · 2024Article
- Human VInternational journal of reproductive biomedicine · 2023Article
- Pattern-recognition receptors in endometriosis: A narrative review.Frontiers in immunology · 2023Review
- CCL20/CCR6 axis mediates macrophages to promote proliferation and migration of ESCs by blocking autophagic flux in endometriosis.Stem cell research & therapy · 2022Article
- Maintenance of Hypoimmunogenic FeaturesFrontiers in bioengineering and biotechnology · 2022Article
- SCM-198 Prevents Endometriosis by Reversing Low Autophagy of Endometrial Stromal CellFrontiers in endocrinology · 2022Article
- Hyaluronic Acid-Modified Nanoplatforms as a Vector for Targeted Delivery of Autophagy-Related Gene to the Endometriotic Lesions in Mice.Frontiers in bioengineering and biotechnology · 2022Article
- miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis.Molecular medicine reports · 2021Article
- Identification and Analysis of Potential Autophagy-Related Biomarkers in Endometriosis by WGCNA.Frontiers in molecular biosciences · 2021Article
- NLRC5 Might Promote Endometrial Cancer Progression by Inducing PD-L1 Expression.Technology in cancer research & treatmentArticle
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nod-like receptor (NLR) family caspase activation and recruitment domain containing 5 (NLRC5) is a newly identified sub-class of the NLR family. It regulates inflammation and has a key function in innate and adaptive immunologic reactions. Autophagy has been reported to be crucially linked to the pathogenesis of endometriosis. Our recent study identify there is a negative correlation between NLRC5 and autophagy in endometriosis, indicating that NLRC5 and autophagy together act as promising predictors in endometriosis patients. However, the mechanism associating NLRC5 and autophagy in endometriosis is still not completely understood. We hypothesize that autophagy could be involved in NLRC5-mediated inflammation in endometriosis. In order to validate the assumption, we evaluate the effects of NLRC5 and autophagy in the inflammation of ectopic endometrial stromal cells (EESCs) of ovarian endometriosis patients, to specifically determine whether autophagy is involved in NLRC5-mediated inflammation in EESCs. Our results show that over-expression of NLRC5 results in the up-regulation of autophagy in EESCs and inhibition of NLRC5 restricts the level of autophagy in EESCs. Furthermore, over-expression of NLRC5 and promotion of autophagy inhibit interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expressions, whereas inhibition of NLRC5 and autophagy up-regulate IL-6 and TNF-α expressions in EESCs. Additionally, promotion of autophagy contributes to the NLRC5-mediated inhibition of IL-6 and TNF-α expressions in EESCs; inhibition of autophagy restricts NLRC5-mediated inhibition of IL-6 and TNF-α expressions in EESCs. Our results suggest that over-expression of NLRC5 promotes autophagy, thereby inhibiting inflammation in ovarian endometriosis.
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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.