In addition, some scholars have found that Hirudin can inhibit fibroblast senescence by promoting the expression of PGC1-α and SIRT3 in fibroblasts, activate the PGC1-α/SIRT3 pathway, and effectively reduce the levels of ROS and oxidative stress markers, thereby exerting an anti-pulmonary fibrosis effect (He et al., 2024a). This evidence concerns the gene PPARGC1A and pulmonary fibrosis.