ArticleCell communication and signaling : CCS2024
Acidic preconditioning induced intracellular acid adaptation to protect renal injury via dynamic phosphorylation of focal adhesion kinase-dependent activation of sodium hydrogen exchanger 1.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed.
- Protective Effect of the NHE1 Inhibitor Buthutin A on Oxidative Stress-Induced Apoptosis in HUVECs.ACS omega · 2026Article
- Integrated bioinformatics and experimental validation reveal that kaempferol ameliorates intervertebral disc degeneration via dual anti-inflammatory and anti-aging pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Valproic Acid Promotes the Differentiation of Satellite Glial Cells into Neurons via the pH-Dependent Pathway.Biomolecules · 2025Article
- Rs9839776 Genetic Variant of lncRNA SOX2OT Contributes to Susceptibility of Acute Kidney Injury in Sepsis Patients via Regulating SOX2OT/miR-9-5p Axis.Journal of inflammation research · 2025Article
- Correction: Acidic preconditioning induced intracellular acid adaptation to protect renal injury via dynamic phosphorylation of focal adhesion kinase-dependent activation of sodium hydrogen exchanger 1.Cell communication and signaling : CCS · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors.
Funding
Abstract
backgroundDisruptions in intracellular pH (pH
methodsAn AP model was established in human kidney (HK2) cells by treating them with an acidic medium for 12 h, followed by a recovery period with a normal medium for 6 h. To induce hypoxia/reoxygenation (H/R) injury, HK2 cells were subjected to hypoxia for 24 h and reoxygenation for 1 h. In vivo, a mouse model of IPC was established by clamping the bilateral renal pedicles for 15 min, followed by reperfusion for 4 days. Conversely, the I/R model involved clamping the bilateral renal pedicles for 35 min and reperfusion for 24 h. Western blotting was employed to evaluate the expression levels of cleaved caspase 3, cleaved caspase 9, NHE1, KIM1, FAK, and NOX4. A pH-sensitive fluorescent probe was used to measure pH
resultsOur findings demonstrated that AP could effectively mitigate H/R injury in HK2 cells. This protective effect and the maintenance of pH
conclusionsThis study provides compelling evidence that AP maintains pH
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Registered trials
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