Pulmonary arterial hypertension is a rare but deadly disease with a complex pathogenesis. Recent evidence demonstrates that Krüppel-like factors, a diverse family of transcription factors, are involved in several key disease processes such as the phenotypic transition of endothelial cells and smooth muscle cells. Importantly, manipulation of certain Krüppel-like factors enables protection or attenuation against pulmonary arterial hypertension in both animal models and preliminary human studies. In this review, we discuss how Krüppel-like factors, in particular Krüppel-like factors 2, 4 and 5 contribute to the pathological phenomena seen in pulmonary arterial hypertension and how associated signaling and microRNA pathways may be suitable targets for new therapies.

肺动脉高压是一种罕见但致命的疾病，发病机制复杂。最近的证据表明，Krüppel 样因子是一个多样化的转录因子家族，参与多种关键疾病过程，例如内皮细胞和平滑肌细胞的表型转变。重要的是，在动物模型和初步人体研究中，操纵某些 Krüppel 样因子可以保护或减弱肺动脉高压。在这篇综述中，我们讨论了 Krüppel 样因子，特别是 Krüppel 样因子 2、4 和 5 如何导致肺动脉高压的病理现象，以及相关信号传导和 microRNA 通路如何成为新疗法的合适靶点。