ArticleCellular and molecular life sciences : CMLS2026
Inflammation-induced LncRNA SNHG1 orchestrates spermatogonium development in non-obstructive azoospermia via IL-17 A signaling pathway.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Non-obstructive azoospermia (NOA) is a critical subtype of male infertility associated with inflammation. However, the molecular mechanisms underlying this phenomenon remain poorly understood. This study investigated the role of the inflammation-activated long non-coding RNA SNHG1 in NOA pathogenesis. Using lipopolysaccharide (LPS)-induced orchitis mouse models and spermatogonium cell lines (GC-1 spg and TCAM-2), we observed that both SNHG1 and the transcription factor SP1 were significantly upregulated, correlating with spermatogonium proliferation and loss of stemness. Mechanistically, SP1 directly binds to and transcriptionally activates the SNHG1 promoter, whereas SNHG1 knockdown rescued LPS-induced spermatogonium dysfunction without affecting SP1 expression. RNA-seq revealed that SNHG1 overexpression activated the IL-17 A signaling pathway. Notably, IL-17 A receptor blockade (Brodalumab) reversed the SNHG1-mediated proliferation arrest and stemness. Our findings demonstrated that the SP1-SNHG1-IL-17 A axis drives inflammatory spermatogenic failure, suggesting IL-17 A inhibition as a potential therapeutic direction.
Indexed as
Identifiers
What OpenQuestion holds
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.