Regulation of inflammation through Mitogen-activated protein kinases

丝裂原活化蛋白激酶（MAPK）如ERK和p38通过信号转导参与炎症和各种生物学现象的调节。为了阐明ERK和p38在体内的功能，我们建立了ERK 2和p38α条件性基因敲除小鼠。对这些小鼠的研究表明，ERK 2和p38α分别参与淋巴细胞发育和代谢综合征的调节。这些结果表明，MAPK通路中的信号分子是控制肥胖诱导的免疫应答和/或慢性炎症的候选靶标。

Mitogen-activated protein kinases (MAPKs) such as ERK and p38 are involved in the regulation of inflammation and various biological phenomena through signal transductions. To elucidate the in vivo functions of ERK and p38, we have established ERK2 and p38α conditional knockout mice. The study of these mice revealed that ERK2 and p38α are involved in the regulation of lymphocyte development and metabolic syndrome, respectively. These results suggest that signaling molecules in the MAPK pathways are candidate targets to control immune responses and/or chronic inflammation induced by obesity.