The cGAS-STING pathway promotes endometriosis by up-regulating autophagy

article OA: closed CC0 ⤵ 5 in-corpus citations
View on OpenAlex View on PubMed View at publisher
AI-generated summary by claude@2026-06, 2026-06-07

The cGAS-STING pathway and autophagy are upregulated in endometriosis, with cGAS-STING promoting disease progression by enhancing autophagy and cell motility.

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

Abstract

OBJECTIVE: To investigate the roles of the cGAS-STING signal pathway and autophagy in the disease progression of endometriosis and to explore the regulatory mechanism of the cGAS-STING signal pathway on autophagy. DESIGN: A case-control experimental study, in vitro primary cell culture study, and in vivo animal research. MAIN OUTCOME MEASURES: Immunohistochemistry, RT-PCR and Western Blot were used to detect cGAS-STING signal pathway and autophagy expression differences in human and rat models. The lentivirus was used to overexpress STING in cells. The expression level of autophagy in human endometrial stromal cells (HESCs) transfected with lv-STING was detected by Western Blot, RT-PCR, and immunofluorescence. Transwell migration and invasion assays were conducted to assess cellular motility. The STING antagonist was applicated in vivo to investigate the therapeutic effects. RESULTS: The expression levels of the cGAS-STING signal pathway and autophagy in Human and Rat ectopic endometrium were increased. STING overexpression promotes the expression of autophagy in human endometrial stromal cells (HESCs). STING overexpression enhances the migration and invasion of the human endometrial stromal cells (HESCs), but the addition of autophagy antagonists could significantly reverse this. STING antagonists inhibited the expression of autophagy in vivo and reduced the volume of ectopic lesions. CONCLUSION: The expression levels of the cGAS-STING signal pathway and autophagy were increased in endometriosis. cGAS-STING signal pathway promotes the development of endometriosis by upregulating autophagy.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Animals Animals Animals Animals Animals

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 (30)

Cited by (5)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-05-11T06:28:56.849735+00:00
pubmed
last seen: 2026-06-01T00:33:58.352283+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK