Cellular and Molecular Aspect of Bladder Pain Syndrome: An Entry Point to Exploration of Its Pathogenesis

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<i>Background:</i> Bladder pain syndrome/interstitial cystitis (BPS/IC) can cause pelvic pain, frequent urination, and a strong urge to urinate. These symptoms can significantly reduce quality of life, causing psychological distress, sexual dysfunction, poor sleep quality, decreased work productivity, and increased morbidity. Despite the prevalence of this condition, determining the most effective treatment guidelines for BPS/IC remains a challenge due to the complexity of its pathogenesis. <i>Objective:</i> Understanding cellular and molecular aspects is essential to explore different cell types in changes in function and sensitivity of the urothelial layer and chronic inflammation. <i>Main Ideas:</i> Cellular aspects in the pathogenesis of BPS/IC include Umbrella Cells, Basal and Intermediate Cells, Paraneuron Cells, Myofibroblasts and Telocytes, Detrusor Smooth Muscle Cells, Nerve Cells, Astrocytes, Microglia, CD68+ Macrophages, CD74+ Lymphocytes, Eosinophils, and Mast Cells. Disruption of these cells leads to altered urothelial barrier function, sensitivity, and chronic inflammation. Molecular aspects include chronic inflammation with increases in p38-mitogen activated protein kinase (p38 MAPK), Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α), Nerve Growth Factor (NGF), Brain-Derived Neurothropic Peptide (BDNF), and other molecules. <i>Conclusion:</i> Changes in the urothelial barrier and bladder wall sensitivity are also significant. Complex interactions between the immune and nervous systems contribute to chronic inflammation through positive feedback. Therefore, this article aims to understand the cellular and molecular aspects that play a role in the pathogenesis of BPS/IC and help provide appropriate treatment.