Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.6.3.1 (
NADPH oxidase
)
11,281
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Acute myocardial infarction (AMI) is the maximum critical cardiovascular event and causes high morbidity and mortality worldwide. The ischemia and reperfusion that occur in AMI cause apoptosis and cellular dysfunction in cardiomyocytes. IL-20, an IL-10 family member, is involved in various inflammatory diseases. Therefore, we sought to elucidate the role of IL-20 in the infarcted heart following ischemia/reperfusion (I/R) injury. We found that IL-20 and its receptors, IL-20R1 and
IL-20R2
, were increased in H2C2 cardiomyoblast cells and ventricular tissues subjected to hypoxia/reoxygenation (H/R) stimulation. The presence of IL-20 further inhibited the cell viability of H9C2 cells and primary cardiomyocytes. Our results suggested that IL-20 elicited an increase in Ca
2+
and activation of the PKC/
NADPH oxidase
pathway, leading to the elevation of oxidase stress and downregulation of AKT. Furthermore, we demonstrated that IL-20 was able to mediate H/R-induced apoptosis via PKC/
NADPH oxidase
/AKT signaling. Our findings implied that IL-20 was responsive to H/R stress in vitro and in rat hearts undergoing I/R injury, and this upregulation of IL-20 may contribute to the apoptosis of cardiomyocytes.
...
PMID:IL-20 promotes hypoxia/reoxygenation-induced mitochondrial dysfunction and apoptosis in cardiomyocytes by upregulating oxidative stress by activating the PKC/NADPH oxidase pathway. 3195 16
