[Interstitial cystitis: the latest findings on its aetiopathogenesis]

New findings provide progress in the understanding of the complicated aetiopathogenesis of interstitial cystitis/bladder pain syndrome (IC/BPS), whose causalities have only been deciphered in fragments so far. An increasingly complex network of pathomechanisms is emerging, in which the frequently mentioned mast cells and urothelial changes seem to be only a fragment of the pathological changes. The latest findings regarding a possible genetic and epigenetic predisposition are based on pedigree analyses, detection of single nucleotide polymorphisms and significant changes in differentially expressed genes. Multiple alterations can be detected at the molecular level. Platelet-activating factor, VEGF, corticotropin-releasing hormone and the inflammasome are important players in understanding the disease, but the pathomechanism underlying the "activation" of IC remains unclear. New starting points could be the detection of viruses (Epstein-Barr virus, BK polyomaviruses) or bacterial inflammation by pathogens that cannot be detected in standard cultures.