Title : HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury.

Pub. Date : 2021 Sep 3

PMID : 34479471






6 Functional Relationships(s)
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1 Our previous studies showed that high-glucose and hypoxic conditions could upregulate HIF-1alpha expression and enhance EC inflammatory injury, independently of the nuclear factor kappa-B (NF-kappaB) pathway. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens
2 RESULTS: High glucose and hypoxia up-regulated HIF-1alpha expression, and down-regulated HIF-1alpha decreased the level of inflammation and oxidative stress in HUVECs. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens
3 RESULTS: High glucose and hypoxia up-regulated HIF-1alpha expression, and down-regulated HIF-1alpha decreased the level of inflammation and oxidative stress in HUVECs. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens
4 Moreover, we observed that HIF-1alpha bound to the promoter of JMJD1A, and the ameliorative effects of si-HIF-1alpha on oxidative stress and inflammatory cytokines in high-glucose and hypoxia-induced HUVECs were reversed by JMJD1A overexpression. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens
5 Moreover, we observed that HIF-1alpha bound to the promoter of JMJD1A, and the ameliorative effects of si-HIF-1alpha on oxidative stress and inflammatory cytokines in high-glucose and hypoxia-induced HUVECs were reversed by JMJD1A overexpression. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens
6 CONCLUSIONS: These findings provide novel evidence that the HIF-1alpha/JMJD1A signaling pathway is involved in inflammation and oxidative stress in HUVECs induced by high glucose and hypoxia. Glucose hypoxia inducible factor 1 subunit alpha Homo sapiens