ArticlePLoS genetics2021
c-Jun N-terminal kinase (JNK) signaling contributes to cystic burden in polycystic kidney disease.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- Kidney-specific deletion of the BicC family RNA-binding protein 1 triggers an ADPKD-like cystogenic program.iScience · 2026Article
- Expression of ERK1/2, p38, and JNK in Normal Kidney Development and CAKUT.Medicina (Kaunas, Lithuania) · 2026Article
- Long-chain polyphosphates induce glomerular microthrombi and exacerbate LPS-induced acute kidney injury in mouse.Disease models & mechanisms · 2026Article
- Role of C-Jun N-Terminal Kinases on a Stressed Epithelium: Time for Testing Isoform Specificity.Biology · 2025Review
- Identification of Associations with Dermatologic Diseases through a Focused GWAS of the UK Biobank.JID innovations : skin science from molecules to population health · 2025Article
- Identification of key necroptosis-related genes and immune landscape in patients with immunoglobulin A nephropathy.BMC nephrology · 2024Article
- The Tumor-Associated Calcium Signal Transducer 2 (TACSTD2) oncogene is upregulated in cystic epithelial cells revealing a potential new target for polycystic kidney disease.PLoS genetics · 2024Article
- TNF-alpha promotes cilia elongation via mixed lineage kinases signaling in mouse fibroblasts and human RPE-1 cells.Cytoskeleton (Hoboken, N.J.) · 2024Article
- JNK regulates ciliogenesis through the interflagellar transport complex and actin networks.The Journal of cell biology · 2023Article
- Polycystin-2-dependent transcriptome reveals early response of autosomal dominant polycystic kidney disease.Physiological genomics · 2023Article
- Article
- Induction of pro-inflammatory genes by fibronectin DAMPs in three fibroblast cell lines: Role of TAK1 and MAP kinases.PloS one · 2023Article
- c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease.Journal of cellular signaling · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people. It primarily is caused by mutations in the transmembrane proteins polycystin-1 (Pkd1) and polycystin-2 (Pkd2). The most proximal effects of Pkd mutations leading to cyst formation are not known, but pro-proliferative signaling must be involved for the tubule epithelial cells to increase in number over time. The c-Jun N-terminal kinase (JNK) pathway promotes proliferation and is activated in acute and chronic kidney diseases. Using a mouse model of cystic kidney disease caused by Pkd2 loss, we observe JNK activation in cystic kidneys and observe increased nuclear phospho c-Jun in cystic epithelium. Genetic removal of Jnk1 and Jnk2 suppresses the nuclear accumulation of phospho c-Jun, reduces proliferation and reduces the severity of cystic disease. While Jnk1 and Jnk2 are thought to have largely overlapping functions, we find that Jnk1 loss is nearly as effective as the double loss of Jnk1 and Jnk2. Jnk pathway inhibitors are in development for neurodegeneration, cancer, and fibrotic diseases. Our work suggests that the JNK pathway should be explored as a therapeutic target for ADPKD.
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