CALD1, also known as Caldesmon 1, plays roles in cell adhesion, cytoskeletal organization, and vascularization [3]. It is associated with multiple signaling pathways such as the PI3K-Akt-mTOR signaling pathway, EMT signaling pathway, and JAK/STAT signaling pathway [2,4]. Abnormal expression of CALD1 has been implicated in various biological processes related to disease development [1-7].

In idiopathic pulmonary fibrosis, CALD1 was identified as a dysregulated hub gene. Knockdown of CALD1 attenuated the expression of fibrotic markers in response to TGF-β1 stimulation in primary fibroblasts, suggesting its contribution to pulmonary fibrosis [1].

In gastric cancer, CALD1-siRNA transfection reduced cell activity, migration, and invasion. Overexpression of CALD1 increased the expression of PI3K-Akt pathway members, and its effect on tumor cell activity, migration, and invasion was weakened by the addition of a PI3K-Akt inhibitor, indicating that CALD1 promotes gastric cancer progression through the PI3K-Akt pathway [2].

In bladder cancer, high expression of CALD1 was significantly correlated with histological grade, clinical stage, and poor prognosis. CALD1 promoted the growth, migration, invasion, and cell cycle of tumor cells, and up-regulated PD-L1 expression via the JAK/STAT signaling pathway [4].

In conclusion, CALD1 is involved in cell-related functions and is associated with multiple diseases including pulmonary fibrosis, gastric cancer, and bladder cancer. Findings from gene knockdown experiments in these disease models have revealed CALD1's role in promoting disease-related processes, providing potential therapeutic targets for these diseases.