ArticleScientific reports2016
The c-Jun N-terminal kinase (JNK) pathway is activated in human interstitial cystitis (IC) and rat protamine sulfate induced cystitis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
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- Inflammation-associated immune-related genes as potential biomarkers for the diagnosis of interstitial cystitis.Clinical and experimental medicine · 2026Article
- A novel prognostic signature based on mitochondrial permeability transition-driven necrosis genes for biochemical recurrence prediction in prostate cancer.Frontiers in oncology · 2026Article
- Exercise Training Promotes Neural Remodeling and Vascular Regeneration in Cerebral Ischemic Rats Through the JNK/c-jun Signaling Pathway.Molecular neurobiology · 2025Article
- Dasatinib inhibits betacoronavirus replication in macrophages and attenuates pro-inflammatory mediators via SRC-MAPK pathway modulation.Medical microbiology and immunology · 2025Article
- Identification and Validation of Biomarkers to Predict Early Diagnosis of Inflammatory Bowel Disease and Its Progression to Colorectal Cancer.Biochemical genetics · 2025Article
- S100A9 as a potential novel target for experimental autoimmune cystitis and interstitial cystitis/bladder pain syndrome.Biomarker research · 2025Article
- Sinapic Acid Ameliorates Cadmium-Induced Hepatotoxicity: Modulation of Oxidative Stress, Inflammation, and Apoptosis.Biomedicines · 2025Article
- Differential influence of 1,8-Cineol on distinct hypoxia-related immune alterations in human monocytes.Scientific reports · 2025Article
- Role of local angiotensin II signaling in bladder function.American journal of physiology. Renal physiology · 2024Review
- SNORC knockdown alleviates inflammation, autophagy defect and matrix degradation of chondrocytes in osteoarthritis development.Molecular and cellular biochemistry · 2024Article
- Mechanisms of oxidative stress in interstitial cystitis/bladder pain syndrome.Nature reviews. Urology · 2024Review
- Chemokine receptor 7 contributes to T- and B-cell filtering in ageing bladder, cystitis and bladder cancer.Immunity & ageing : I & A · 2024Article
- Unraveling the complex roles of macrophages in obese adipose tissue: an overview.Frontiers of medicine · 2024Review
- Serpina3n/serpina3 alleviates cyclophosphamide-induced interstitial cystitis by activating the Wnt/β-catenin signal.International urology and nephrology · 2023Article
- Caffeic acid methyl ester inhibits mast cell activation through the suppresion of MAPKs and NF-κB signaling in RBL-2H3 cells.Heliyon · 2023Article
- 3,4,5‑Trihydroxycinnamic acid suppresses phorbol‑12‑myristate‑13‑acetate and A23187‑induced mast cell activation in RBL‑2H3 cells.Experimental and therapeutic medicine · 2023Article
- Decreased autophagic activity of detrusor cells is involved in the inflammatory response of interstitial cystitis/bladder pain syndrome.International urogynecology journal · 2023Article
- Changes in nerve growth factor signaling in female mice with cyclophosphamide-induced cystitis.Frontiers in urology · 2023Article
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9 authors at 3 institutions in 1 country.
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Abstract
The pathogenesis of bladder pain syndrome/interstitial cystitis (BPS/IC) is currently unclear. However, inflammation has been suggested to play an important role in BPS/IC. JNK downstream signaling plays an important role in numerous chronic inflammatory diseases. However, studies of the JNK pathway in BPS/IC are limited. In this study, we investigated the role of the JNK pathway in human BPS/IC and rat protamine sulfate (PS)-induced cystitis and examined the effect of the selective JNK inhibitor SP600125 on rat bladder cystitis. In our study, we demonstrated that the JNK signaling pathway was activated (the expression of JNK, c-Jun, p-JNK, p-c-Jun, IL-6 and TNF-α were significantly increasing in BPS/IC compared to the non-BPS/IC patients) and resulted in inflammation in human BPS/IC. Further animal models showed that the JNK pathway played an important role in the pathogenesis of cystitis. JNK inhibitors, SP600125, effectively inhibited the expression of p-JNK, p-c-Jun, IL-6 and TNF-α. The inhibition of these pathways had a protective effect on PS-induced rat cystitis by significantly decreasing histological score and mast cell count and improving bladder micturition function (micturition frequency significantly decreasing and bladder capacity significantly increasing). Therefore, JNK inhibition could be used as a potential treatment for BPS/IC.
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