ArticleDiabetes & metabolism journal2026
STING Promotes Renal Fibrosis in Diabetic Kidney Disease via ID1-Dependent Epithelial-Mesenchymal Transition.
Article in Diabetes & metabolism journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The Role and Therapeutic Potential of the STING Signaling Pathway in the Pathogenesis of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgruoundTubulointerstitial fibrosis (TIF) due to epithelial-mesenchymal transition (EMT) is an inseparable feature of diabetic renal fibrosis. Although stimulator of interferon genes (STING) has been shown to play a potential role in regulating EMT, whether and how it modulates EMT in diabetic kidney disease (DKD) mice remain unclear. Here, we investigated the role and underlying mechanisms of STING-mediated EMT in TIF in DKD.
methodsSTING expression was detected in human renal biopsy tissues and serum samples from patients with DKD. Mouse models with genetic STING deletion or pharmacological by a STING inhibitor (C176) were established to further investigate the functions of STING in vivo. The in vitro roles of STING were analyzed in human renal tubular epithelial (HK2) cells with STING overexpression or knockdown. RNA sequencing was used to explore the underlying mechanisms.
resultsSTING was upregulated in the kidneys and serum of patients with DKD and was negatively correlated with kidney function. STING deletion or pharmacological inhibition with C176 ameliorated pathological lesions, renal dysfunction and fibrosis in mouse models of DKD. STING deficiency alleviated renal fibrosis in DKD mice by inhibiting EMT. Mechanistically, RNA sequencing identified, inhibitor of differentiation 1 (ID1) as a downstream molecule of STING. Inhibition of ID1 in the setting of STING overexpression suppressed EMT and renal fibrosis.
conclusionOur study provides evidence that STING deficiency relieves renal fibrosis by inhibiting ID1-mediated EMT and that inhibition of STING and ID1 has therapeutic potential for patients with DKD.
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.