Cald1, also known as Caldesmon 1, is involved in cell adhesion, cytoskeletal organization, and vascularization [3]. It may be associated with several signaling pathways, such as the PI3K-Akt-mTOR signaling pathway, EMT signaling pathway, JAK/STAT signaling pathway, and MAPK pathway [2,5,6]. Cald1 plays a role in many cellular functions and is of great biological importance in various physiological and pathological processes [4].

In idiopathic pulmonary fibrosis, knockdown of Cald1 attenuated the expression of fibrotic markers in primary fibroblasts, suggesting its potential role in promoting pulmonary fibrosis [1]. In gastric cancer, CALD1-siRNA transfection reduced cell activity, migration, and invasion abilities, and upregulation of CALD1 affected the expression of PI3K-Akt pathway-related proteins, indicating that increased CALD1 expression promotes GC progression, invasion, and metastasis by regulating the PI3K-Akt pathway to promote EMT [2]. In bladder cancer, high expression of CALD1 was associated with poor prognosis, and it promoted the malignant progression of BC and upregulated PD-L1 expression via the JAK/STAT signaling pathway [5]. In ovarian cancer, high expression of CALD1 was associated with disease stage, venous invasion, and poor prognosis under platinum drug intervention, suggesting it could be a target for platinum-resistance mechanism study [7].

In conclusion, Cald1 is involved in multiple cellular functions and signaling pathways. Through gene-knockout or knockdown experiments in different disease models, Cald1 has been shown to play important roles in various diseases, including pulmonary fibrosis, gastric cancer, bladder cancer, and ovarian cancer. These findings contribute to understanding the mechanisms of these diseases and provide potential therapeutic targets.