Klf11, also known as Krüppel-like factor 11, is involved in multiple biological functions and associated with various pathways. It has been implicated in maintaining vascular homeostasis, and missense mutations in KLF11 can lead to diabetes in humans [2,3]. Klf11 is also related to processes like ferroptosis, a form of iron-dependent non-apoptotic cell death, which is crucial in tumor proliferation and chemotherapy resistance [1].

In various disease models, Klf11 shows distinct functions. In lung adenocarcinoma, overexpression of Klf11 promotes ferroptosis, inhibits cell proliferation, and increases chemosensitivity by suppressing GPX4, while knockout has the opposite effect [1]. In endothelial-specific models, Klf11 deficiency accelerates atherogenesis in diabetic conditions, while overexpression inhibits it, with loss of Klf11 increasing endothelial-to-mesenchymal transition (EndMT) [2]. In a murine deep vein thrombosis model, conventional Klf11 knockout mice are more susceptible to developing stasis-induced DVT, as Klf11 downregulates tissue factor gene transcription under prothrombotic conditions [3]. In glioma, knockdown of Klf11 inhibits cell proliferation and migration, and reduces tumor size in vivo [5]. In breast cancer, KLF11 promotes cell proliferation by inhibiting p53-MDM2 signaling [4]. Also, in sorafenib-induced cardiotoxicity, KLF11 promotes ferroptosis by suppressing transcription of ferroptosis suppressor protein 1 (FSP1) [6].

In conclusion, Klf11 has diverse biological functions. Its role in promoting ferroptosis, regulating cell proliferation, and affecting vascular-related processes is well-demonstrated through gene knockout and other functional studies in multiple disease areas such as cancer, cardiovascular diseases, and thrombosis. These model-based studies help in understanding the molecular mechanisms underlying these diseases and potentially identifying new therapeutic targets [1,2,3,4,5,6].