Cemip, also known as KIAA1199 and HYBID, is a member of the hyaluronidase family. It degrades hyaluronic acid (HA) in the extracellular matrix and remodels it, and is involved in regulating several signaling pathways such as WNT and EGFR [2,4,5,6]. Cemip plays a crucial role in various biological processes and diseases, including tumor initiation and progression, arthritis, atherosclerosis, and idiopathic pulmonary fibrosis [3,4]. Genetic models like KO/CKO mouse models can be valuable for further exploring its functions.

In tumor-related studies, Cemip overexpression is significantly associated with poor overall survival (OS) and disease-free survival (DFS) in cancer patients. It is related to advanced clinical stage, lymph node metastasis, and poor histological grade in multiple cancers [1]. In small-cell lung cancer (SCLC), Cemip-mediated HA degradation activates the TLR2/c-Src/ERK1/2 axis, promoting SCLC metastasis, and Cemip depletion attenuated metastasis in SCLC xenografts [7].

In cardiac remodeling post-myocardial infarction, Cemip promotes TSP4 degradation in an ACTN4-dependent manner, activating the FAK signaling pathway, and Cemip knockdown in mice reduced cardiac fibrosis and improved cardiac function [8].

In conclusion, Cemip is essential in extracellular matrix remodeling through HA degradation and is involved in multiple disease-related biological processes. KO/CKO mouse models have provided insights into its role in cancer metastasis and cardiac remodeling post-myocardial infarction, helping to understand disease mechanisms and potentially identify new therapeutic targets.