ArticleCell cycle (Georgetown, Tex.)2014
Role of CDK5/cyclin complexes in ischemia-induced death and survival of renal tubular cells.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 12 citations in OpenAlex.
- Dexmedetomidine ameliorates high glucose-induced epithelial-mesenchymal transformation in HK-2 cells through the Cdk5/Drp1/ROS pathway.Acta biochimica et biophysica Sinica · 2024Article
- Histone deacetylase inhibitor pracinostat suppresses colorectal cancer by inducing CDK5-Drp1 signaling-mediated peripheral mitofission.Journal of pharmaceutical analysis · 2023Article
- TFP5-Mediated CDK5 Activity Inhibition Improves Diabetic NephropathyFrontiers in cell and developmental biology · 2022Article
- The role of PAK1 in the sensitivity of kidney epithelial cells to ischemia-like conditions.Cell cycle (Georgetown, Tex.) · 2019Article
- Cdk5 links with DNA damage response and cancer.Molecular cancer · 2017Review
- DNA damage response in nephrotoxic and ischemic kidney injury.Toxicology and applied pharmacology · 2016Review
- CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPARγ pathway.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia reperfusion processes induce damage in renal tubules and compromise the viability of kidney transplants. Understanding the molecular events responsible for tubule damage and recovery would help to develop new strategies for organ preservation. CDK5 has been traditionally considered a neuronal kinase with dual roles in cell death and survival. Here, we demonstrate that CDK5 and their regulators p35/p25 and cyclin I are also expressed in renal tubular cells. We show that treatment with CDK inhibitors promotes the formation of pro-survival CDK5/cyclin I complexes and enhances cell survival upon an ischemia reperfusion pro-apoptotic insult. These findings support the benefit of treating with CDK inhibitors for renal preservation, assisting renal tubule protection.
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Registered trials
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