Ptx3, also known as long pentraxin 3, is a soluble pattern recognition molecule belonging to the humoral innate immune system [2,3,4]. It is rapidly produced at inflammatory sites by phagocytes and stromal cells in response to infection or tissue injury. Ptx3 interacts with various molecules such as microbial moieties, components of the complement and hemostatic systems, and extracellular matrix components. It plays a crucial role in innate immunity, inflammation, and tissue repair, and has been associated with multiple biological processes including neovascularization, energy metabolism, invasion, and metastasis [1,2]. Genetic models like gene-knockout (KO) mouse models have been valuable in studying Ptx3.

In Ptx3-deficient mice, there are several notable phenotypes. In the context of idiopathic pulmonary fibrosis, PTX3-deficiency was associated with worsening of the disease, impaired fibrin removal, and increased collagen deposition, suggesting a protective role of PTX3 in tissue repair [2]. In bone-related studies, Ptx3-targeted mice exhibit reduced trabecular volume during bone development and impaired callus mineralization following experimental fracture [3]. Regarding the lymphatic vasculature, Ptx3-deficient mice showed lymphatic vessel (LV) abnormalities in the colon submucosa and diaphragm, defective fluid drainage from footpads, and defective dendritic cell trafficking, indicating PTX3's role in the structural organization and immunological function of specialized LV [5].

In conclusion, Ptx3 is an essential molecule in multiple biological processes. Model-based research, especially using Ptx3 KO mouse models, has revealed its roles in diseases such as idiopathic pulmonary fibrosis, bone-related pathologies, and lymphatic-associated disorders. These findings contribute to our understanding of the underlying mechanisms of these diseases and may potentially lead to new therapeutic strategies targeting Ptx3.