ArticleCellular and molecular life sciences : CMLS2025
IER3 drives the transition from sepsis-associated AKI to CKD by suppressing the mitochondrial translocation of PRDX5.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Mechanisms of salvianolic acids in kidney disease therapy: advances and perspectives.Frontiers in pharmacology · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Sepsis-associated acute kidney injury (SAKI) is a severe condition associated with high mortality and long-term complications. Currently, there is no effective strategy to halt AKI chronicization. Stress-induced senescence of renal tubular epithelial cells (RTECs) is a pivotal driving mechanism in the AKI-CKD transition. Previous scRNA-seq revealed that the expression of immediate early response gene 3 (IER3) was markedly upregulated in the senescent RTECs of patients with AKI and that the IER3
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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.