Klf7, also known as Kruppel-like factor 7, is a transcriptional activator. It is involved in multiple biological processes and disease-related pathways. In adipocytes, it activates the PKCζ/NF-κB pathway, promoting inflammation and glucose metabolism disorder [4]. In osteoclasts, it promotes differentiation by suppressing HO-1, which may be related to osteoporosis [5].

In cancer research, gene-editing mouse models have been used to study Klf7. In male mice, cardiac-specific knockout of Klf7 induces adult concentric hypertrophy by regulating glycolysis and fatty acid oxidation fluxes [2]. In hepatocellular carcinoma (HCC), genetic depletion of Klf7 impedes HMGB1-mediated HCC progression and metastasis, as Klf7 overexpression promotes HCC metastasis through transactivating TLR4 and PTK2 [1]. In colon adenocarcinoma, KLF7 knockdown attenuated the growth and metastasis of COAD both in vitro and in vivo, as KLF7 promotes COAD progression through the PDGFB signaling pathway [3].

In conclusion, Klf7 plays crucial roles in metabolism-related processes like cardiac metabolic remodeling and adipocyte function, as well as in disease-promoting processes such as cancer progression and osteoporosis development. The use of gene knockout or conditional knockout mouse models has been instrumental in revealing these functions, providing insights into potential therapeutic strategies for related diseases.