Chemokine CCL21 promotes the pathological progression of endometriosis by regulating inflammatory cytokine expression and activating the NF-κB signaling pathway

Wang N, Ning Wang, Liu B, Bo Liu, Yiyuan Zhang, Zhang Y, Xiao-hua Man, Xiaoqian Man, Man X, Jiang R, Rujiao Jiang, Yao L, Liang Yao, Dong X, Xiaoying Dong, Meihua Guo, Guo M, Sun J, Jie Sun, Bi J, Jianlei Bi
International Immunopharmacology · 2026 · vol. 186 , pp. 117079 · doi:10.1016/j.intimp.2026.117079 · PMID:42372587 · W7166567596
article OA: closed public-domain-us
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-17 ⓘ

Chemokine CCL21 promotes endometriosis progression by increasing inflammatory cytokines like IL-6, IL-1β, and TNF-α via NF-κB pathway activation.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis, affecting approximately 10% of reproductive-aged women worldwide, is widely recognized as a chronic inflammatory disease. Inflammation-related genes (IRGs) play a crucial role in the occurrence and progression of various diseases, including endometriosis. However, identifying the key IRGs that drive endometriosis pathologyand whether they can be therapeutically targeted remains unclear. In the present study, the ectopic endometrium (EcE) and eutopic endometrium (EuE) from endometriosis patients were collected and a mouse model of endometriosis was established to investigate the expression levels of inflammatory factors. Three hub IRGs (CCL21, CFD, and ACKR1) in endometriosis were identified, which were able to accurately predict the occurrence of endometriosis. The expression of CCL21 was significantly increased in the EcE in EcE from patients with endometriosis and in endometriosis-like lesions from mice. Knockdown of CCL21 inhibited the proliferation, migration, and invasion of 12z cells and promoted apoptosis. Mechanistically, CCL21 knockdown attenuated endometriosis-associated inflammatory signaling through restraining the activation of the NF-κB signaling pathway and the downstream inflammatory factors (IL-6, IL-1β, and TNF-α). In conclusion, increased CCL21 promoted the development of endometriosis by regulating inflammatory cytokine and activating the NF-κB signaling pathway. This finding offers a novel therapeutic target for treatment.

My notes (saved in your browser only)

MeSH descriptors

Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Chemokine CCL21 Cytokines

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (38)

SciLite annotations

organisms 3
noordeloos 2009062 transgenic mice mus sp.

Source provenance

europepmc
last seen: 2026-08-26T06:08:41.316361+00:00
openalex
last seen: 2026-08-26T06:01:51.998721+00:00
pubmed
last seen: 2026-08-26T06:03:45.274022+00:00
scilite
last seen: 2026-07-12T09:48:33.364277+00:00
unpaywall
last seen: 2026-08-25T06:41:39.333708+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine