ArticleOncotarget2017
Pharmacological inhibition of Src kinase protects against acute kidney injury in a murine model of renal ischemia/reperfusion.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025Review
- Pharmacological inhibition of Src family kinases attenuates hyperuricemic nephropathy.Frontiers in pharmacology · 2024Article
- The role of non-protein-coding RNAs in ischemic acute kidney injury.Frontiers in immunology · 2024Review
- Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress.BMC molecular and cell biology · 2023Article
- Src Family Kinases: A Potential Therapeutic Target for Acute Kidney Injury.Biomolecules · 2022Review
- LncRNA TUG1 regulates the development of ischemia-reperfusion mediated acute kidney injury through miR-494-3p/E-cadherin axis.Journal of inflammation (London, England) · 2021Article
- Renal Tubular Epithelial TRPA1 Acts as An Oxidative Stress Sensor to Mediate Ischemia-Reperfusion-Induced Kidney Injury through MAPKs/NF-κB Signaling.International journal of molecular sciences · 2021Article
- Gene deficiency or pharmacological inhibition of PDCD4-mediated FGR signaling protects against acute kidney injury.Acta pharmaceutica Sinica. B · 2021Article
- KF-1607, a Novel Pan Src Kinase Inhibitor, Attenuates Obstruction-Induced Tubulointerstitial Fibrosis in Mice.Biomolecules & therapeutics · 2021Article
- Inhibition of Src Family Kinases Ameliorates LPS-Induced Acute Kidney Injury and Mitochondrial Dysfunction in Mice.International journal of molecular sciences · 2020Article
- Effect of GM6001 on the expression of syndecan-1 in rats with acute kidney injury and its protective effect on the kidneys.Experimental and therapeutic medicine · 2020Article
- Fyn Kinase: A Potential Therapeutic Target in Acute Kidney Injury.Biomolecules & therapeutics · 2020Review
- Effects of Rab7 gene up-regulation on renal fibrosis induced by unilateral ureteral obstruction.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Tubular injury triggers podocyte dysfunction by β-catenin-driven release of MMP-7.JCI insight · 2019Article
- Learning important features from multi-view data to predict drug side effects.Journal of cheminformatics · 2019Article
- The role of PAK1 in the sensitivity of kidney epithelial cells to ischemia-like conditions.Cell cycle (Georgetown, Tex.) · 2019Article
- Restoration of E-cadherin by PPBICA protects against cisplatin-induced acute kidney injury by attenuating inflammation and programmed cell death.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Hypoxia Activates Src and Promotes Endocytosis Which Decreases MMP-2 Activity and Aggravates Renal Interstitial Fibrosis.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Activation of Src kinase has been implicated in the pathogenesis of acute brain, liver, and lung injury. However, the role of Src in acute kidney injury (AKI) remains unestablished. To address this, we evaluated the effects of Src inhibition on renal dysfunction and pathological changes in a murine model of AKI induced by ischemia/reperfusion (I/R). I/R injury to the kidney resulted in increased Src phosphorylation at tyrosine 416 (activation). Administration of PP1, a highly selective Src inhibitor, blocked Src phosphorylation, improved renal function and ameliorated renal pathological damage. PP1 treatment also suppressed renal expression of neutrophil gelatinase-associated lipocalin and reduced apoptosis in the injured kidney. Moreover, Src inhibition prevented downregulation of several adherens and tight junction proteins, including E-cadherin, ZO-1, and claudins-1/-4 in the kidney after I/R injury as well as in cultured renal proximal tubular cells following oxidative stress. Finally, PP1 inhibited I/R-induced renal expression of matrix metalloproteinase-2 and -9, phosphorylation of extracellular signal-regulated kinases1/2, signal transducer and activator of transcription-3, and nuclear factor-κB, and the infiltration of macrophages into the kidney. These data indicate that Src is a pivotal mediator of renal epithelial injury and that its inhibition may have a therapeutic potential to treat AKI.
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Registered trials
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