信号转导
细胞生物学
氧化应激
活性氧
MAPK/ERK通路
下调和上调
一氧化氮合酶
超氧化物歧化酶
细胞信号
化学
一氧化氮
兴奋
NF-κB
骨骼肌
激酶
生物
生物化学
内分泌学
基因
作者
Li Li Ji,Mari Carmen Gómez-Cabrera,José Viña
标识
DOI:10.1196/annals.1354.061
摘要
Abstract: Contraction‐induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) κB and mitogen‐activated protein kinases (MAPKs) are the major oxidative stress–sensitive signal transduction pathways in mammalian tissues. Activation of NF‐κB signaling cascade has been shown to enhance the gene expression of important enzymes, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). MAPK activations are involved in a variety of cellular functions including growth, proliferation, and adaptation. We investigated the effect of an acute bout of exercise on NF‐κB and MAPK signaling, as well as on the time course of activation, in rat skeletal muscle. In addition, we studied the role of ROS in the exercise‐induced upregulation of MnSOD and iNOS, and the potential interactions of NF‐κB and MAPK in the signaling of these enzymes. Our data suggest that ROS may serve as messenger molecules to activate adaptive responses through these redox‐sensitive signaling pathways to maintain cellular oxidant‐antioxidant homeostasis during exercise.
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