ArticleEuropean journal of medical research2025
Serum response factor targets Cyr61 to facilitate chronic progression after ischemic acute kidney injury through renal tubular epithelial-myofibroblast transdifferentiation.
Article in European journal of medical research, 2025. 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
13 authors.
Funding
Abstract
objectivesTo explore the regulation and function of serum response factor (SRF)/cysteine-rich protein 61 (Cyr61) pathway in renal tubular epithelial-myofibroblast transdifferentiation (EMyT) in the chronic progression after ischemic acute kidney injury (AKI).
methodsThe expression of SRF, Cyr61, myofibroblast markers (collagen-3, α-SMA and vimentin) and epithelial markers (E-cadherin and ZO-1) were examined in mouse renal tubular epithelial cells (TCMK-1 cells) under hypoxia/reoxygenation (H/R) treatment or rat renal medulla tissue samples after ischemia/reperfusion (I/R) treatment. SRF was overexpressed by pcDNA-SRF plasmid and suppressed by CCG-1423 (a small molecule inhibitor of SRF) or SRF siRNA to study how SRF influences renal tubular EMyT through Cyr61 in the chronic progression after AKI.
resultsIn TCMK-1 cells under H/R treatment and renal medulla tissue from I/R rats, the SRF along with Cyr61, collagen-3, α-SMA and vimentin expression was upregulated, while E-cadherin and ZO-1 expression was downregulated. SRF upregulation in TCMK-1 cells increased Cyr61 expression. Blockade of SRF by an SRF-specific siRNA or CCG-1423 reduced Cyr61 induction, protected renal tubular epithelial cells from undergoing EMyT and improved the chronic progression after ischemic AKI both in vitro and in vivo.
conclusionsIncreased SRF/Cyr61 pathway activity promotes EMyT and dysfunction in renal tubular epithelial cells in the chronic progression after AKI. Targeting SRF with CCG-1423 may be an attractive therapeutic strategy in the chronic progression after AKI.
Indexed as
Identifiers
What Socratic 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 Socratic graph.