ReviewFrontiers in physiology2017
The JNK Signaling Pathway in Renal Fibrosis.
Review in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
115 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.
- Multifunctionality of Calebin A in inflammation, chronic diseases and cancer.Frontiers in oncology · 2022Pooled it
- Multifactorial mechanisms of 5-fluorouracil-induced cardiotoxicity and the cardioprotective role of gallic acid.Molecular biology reports · 2026Article
- Inhibition of the 4-hydroxynonenal-regulated JNK/c-Jun pathway improves bleomycin-induced lung fibrosis.Biomedical journal · 2026Article
- Research Progress of Treatment of Gouty Arthritis with Chinese Medicine Based on Signal Pathways.Chinese journal of integrative medicine · 2026Review
- Protective role of Boerhavia diffusa root extract in methotrexate-induced renal injury: evidence from oxidative stress, molecular, and immunohistochemical markers.BMC complementary medicine and therapies · 2026Article
- Expression of ERK1/2, p38, and JNK in Normal Kidney Development and CAKUT.Medicina (Kaunas, Lithuania) · 2026Article
- Integrated Virtual Screening Approaches to Identify Novel N- Substituted Heterocyclic Compounds as MAPK Inhibitors for Neuro Inflammation.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2026Article
- The subcellular localization-dependent dual role of NR4A1 in renal fibrosis: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- RNA Sequencing Analyses and Validation of Immune-Related Genes in EBV-Specific Cytotoxic T Lymphocytes During Latent Infection.ImmunoTargets and therapy · 2026Article
- Leucine Mitigates Diabetic Nephropathy via Its Antioxidant Effect and Modulation of TGF-β/SMAD-3 Signalling Pathway in Streptozotocin-Induced Diabetic Rats.Drug design, development and therapy · 2026Article
- Intermodulation of endoplasmic reticulum stress and ferroptosis in diabetic nephropathy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025Review
- Fused in Sarcoma (FUS) promotes renal cell carcinoma progression via the KCMF1/FUS/CENPT axis and activation of the JNK signaling pathway.Journal of translational medicine · 2025Article
- Erythropoiesis-Stimulating Agent Protects Against Kidney Fibrosis by Inhibiting G2/M Cell Cycle Arrest.Cells · 2025Article
- Modulation of renal fibrosis-related signaling pathways by traditional Chinese medicine: molecular mechanisms and experimental evidence.International urology and nephrology · 2025Review
- Advances in JNK inhibitor development: therapeutic prospects in neurodegenerative diseases and fibrosis.Archives of pharmacal research · 2025Review
- Evolving adeno-associated viruses for gene transfer to the kidney via cross-species cycling of capsid libraries.Nature biomedical engineering · 2025Article
- HBV promotes epithelial-mesenchymal transition in HCC and liver fibrosis through JNK-mediated autophagy.Hepatology communications · 2025Article
- Role of C-Jun N-Terminal Kinases on a Stressed Epithelium: Time for Testing Isoform Specificity.Biology · 2025Review
- Microarray analysis of the effects of Acthar Gel versus methylprednisolone in a model of focal segmental glomerulosclerosis in female rats.Physiological reports · 2025Article
- Glial cell line-derived neurotrophic factor and its role in attenuating renal fibrosis: a review.The Korean journal of internal medicine · 2025Review
55 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis of the glomerular and tubulointerstitial compartments is a common feature of chronic kidney disease leading to end-stage renal failure. This fibrotic process involves a number of pathologic mechanisms, including cell death and inflammation. This review focuses on the role of the c-Jun amino terminal kinase (JNK) signaling pathway in the development of renal fibrosis. The JNK pathway is activated in response to various cellular stresses and plays an important role in cell death and inflammation. Activation of JNK signaling is a common feature in most forms of human kidney injury, evident in both intrinsic glomerular and tubular cells as well as in infiltrating leukocytes. Similar patterns of JNK activation are evident in animal models of acute and chronic renal injury. Administration of JNK inhibitors can protect against acute kidney injury and suppress the development of glomerulosclerosis and tubulointerstitial fibrosis. In particular, JNK activation in tubular epithelial cells may be a pivotal mechanism in determining the outcome of both acute kidney injury and progression of chronic kidney disease. JNK signaling promotes tubular epithelial cell production of pro-inflammatory and pro-fibrotic molecules as well as tubular cell de-differentiation toward a mesenchymal phenotype. However, the role of JNK within renal fibroblasts is less well-characterized. The JNK pathway interacts with other pro-fibrotic pathways, most notable with the TGF-β/SMAD pathway. JNK activation can augment TGF-β gene transcription, induce expression of enzymes that activate the latent form of TGF-β, and JNK directly phosphorylates SMAD3 to enhance transcription of pro-fibrotic molecules. In conclusion, JNK signaling plays an integral role in several key mechanisms operating in renal fibrosis. Targeting of JNK enzymes has therapeutic potential for the treatment of fibrotic kidney diseases.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.