Krüppel-like factor 2 (KLF2)

Krüppel-like factor 2 (KLF2) is a zinc finger transcription factor in the Krüppel-like factor family and plays a central role in the regulation of cell differentiation, quiescence, proliferation, adhesion, and migration across diverse cell types[1][3]. It was first described as lung Krüppel-like factor due to high expression in lung tissue, but it is also critical for vascular homeostasis, especially in endothelial cells, where it responds to laminar shear stress and is induced by drugs such as statins[2][3]. KLF2 is essential for normal embryonic development, notably vascular development, and regulates immune cell (B and T cell) differentiation, migration, and activation. Its loss contributes to diseases such as atherosclerosis, cardiovascular disease, and lymphoid malignancies like splenic marginal zone lymphoma and multiple myeloma[1][2][3]. KLF2 exerts anti-inflammatory and anti-thrombotic effects in endothelial cells, and its modulation is a mechanism of action for certain cardiovascular drugs such as statins[2].

Other names

Lung Krüppel-like factorLKLF

Induction of KLF2 enhances endothelial function, reduces pro-inflammatory gene expression, and induces anti-thrombotic pathways; therapeutic strategies may target KLF2 for vascular protection or regulation of immune cell function