It is increasingly clear that inflammatory diseases and cancers are influenced by cleavage products of the pro-hormone chromogranin A (CgA), such as the 21-amino acids long catestatin (CST). The goal of this review is to provide an overview of the anti-inflammatory effects of CST and its mechanism of action. We discuss evidence proving that CST and its precursor CgA are crucial for maintaining metabolic and immune homeostasis. CST could reduce inflammation in various mouse models for diabetes, colitis and atherosclerosis. In these mouse models, CST treatment resulted in less infiltration of immune cells in affected tissues, although in vitro monocyte migration was increased by CST. Both in vivo and in vitro, CST can shift macrophage differentiation from a pro- to an anti-inflammatory phenotype. Thus, the concept is emerging that CST plays a role in tissue homeostasis by regulating immune cell infiltration and macrophage differentiation. These findings warrant studying the effects of CST in humans and make it an interesting therapeutic target for treatment and/or diagnosis of various metabolic and immune diseases.
越来越明显的是,炎症性疾病和癌症受到促激素嗜铬粒蛋白A(CgA)裂解产物的影响,比如由21个氨基酸组成的长链儿茶酚抑素(CST)。本综述的目的是概述CST的抗炎作用及其作用机制。我们讨论了证明CST及其前体CgA对维持代谢和免疫内稳态至关重要的证据。CST能够减轻糖尿病、结肠炎和动脉粥样硬化等多种小鼠模型中的炎症。在这些小鼠模型中,CST治疗导致受影响组织中免疫细胞的浸润减少,尽管在体外CST会增加单核细胞的迁移。在体内和体外,CST都能使巨噬细胞的分化从促炎表型转变为抗炎表型。因此,一种观点逐渐形成,即CST通过调节免疫细胞浸润和巨噬细胞分化在组织内稳态中发挥作用。这些发现使得有必要研究CST在人体中的作用,并使其成为治疗和/或诊断各种代谢和免疫疾病的一个有吸引力的治疗靶点。