Angptl2-KO Mouse

Angptl2, or Angiopoietin-like protein 2, is a secreted glycoprotein and a member of the angiopoietin-like protein family. It has diverse functions including being involved in angiogenesis, hematopoiesis, and tumorigenesis. It exerts effects via receptors such as integrin α5β1, LILRB2, and MAG, and is associated with multiple signaling pathways like MAPKs, Akt, NF-κB, and DUSP1 pathway [2,3,5,6,7]. It is of great biological importance as it is implicated in various physiological and pathological processes [5].

In a mouse model of ICI-related autoimmune myocarditis, ANGPTL2 deficiency attenuated autoimmune inflammation, with decreased T cells and macrophages. Cardiac myofibroblast-derived ANGPTL2 enhanced chemoattractant expression via the NF-κB pathway, accelerating T cell recruitment into heart tissues [1]. In doxorubicin-induced cardiotoxicity in mice, ANGPTL2 overexpression exacerbated cardiac dysfunction, apoptosis, and oxidative stress, while its knockdown alleviated these effects through the DUSP1 pathway [3]. In acute lung injury mouse models, ANGPTL2 knockout alleviated LPS-induced pathological symptoms, reduced inflammation, and modulated alveolar macrophage polarization [4].

In conclusion, Angptl2 plays crucial roles in inflammation, cardiac function, and immune-related processes. Studies using gene knockout mouse models have revealed its significance in diseases such as autoimmune myocarditis, doxorubicin-induced cardiotoxicity, and acute lung injury, providing insights into disease mechanisms and potential therapeutic targets.