6533b872fe1ef96bd12d4079
RESEARCH PRODUCT
Redox Regulation by HGF/c-Met in Liver Disease
Ma.concepción Gutiérrez-ruizV.m. FactorSnorri S. ThorgeirssonJens U. MarquardtLuis Enrique Gómez-quirozsubject
0301 basic medicinechemistry.chemical_classificationReactive oxygen speciesC-MetNADPH oxidaseCellBiologymedicine.disease_causeCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structurechemistrymedicinebiology.proteinHepatocyte growth factorReceptor030217 neurology & neurosurgeryOxidative stressHomeostasismedicine.drugdescription
Reactive oxygen species (ROS) have gained considerable attention in recent years because of their direct involvement in the regulation of multiple physiological and pathological processes. Under normal conditions, ROS have an important role in cell signaling and function as essential mediators of cell homeostasis. However, imbalance between ROS and antioxidant systems induces oxidative stress, which leads to cell and tissue damage. The cellular redox modulation by hepatocyte growth factor (HGF) and its receptor c-Met in the liver has been studied extensively in the past. The generation of liver-specific c-Met–knockout mice has allowed to demonstrate the fundamental importance of HGF/c-Met in the control of cellular redox state by regulating the expression of antioxidant proteins and a parallel inhibition of pro-oxidant systems. In this chapter we summarize and discuss the findings regarding the role of HGF/c-Met in modulation of redox state and resistance to oxidative stress.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2017-01-01 |