This review compiles the current knowledge on the effects of prostanoids - arachidonic acid metabolites - on their own synthesis, activity and degradation. Interaction mechanisms between the receptors for the relevant compounds are presented, in particular with regard to the cooperation between a thromboxane A₂ and prostaglandin I₂ receptors. The questions of desensitization and internalization of receptors are discussed. The stages of the inflammatory response and tumor progression are analyzed against the background of the disruption of the synthesis of prostanoids. Special attention is given to the significance of 15-deoxy-Δ(12,14)-prostaglandin J₂ in the regulation of the synthesis of prostanoids and its role as an anti-inflammatory agent. Ultimately, therapeutic approaches as used in various treatments are discussed in the light of the available knowledge.