ArticleMediators of inflammation2014
Myeloid knockout of HIF-1 α does not markedly affect hemorrhage/resuscitation-induced inflammation and hepatic injury.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting Kupffer Cell Enolase 1 Attenuates Liver Inflammation and Injury in Hemorrhagic Shock.International journal of molecular sciences · 2025Article
- MKK4 Knockdown Plays a Protective Role in Hemorrhagic Shock-Induced Liver Injury through the JNK Pathway.Oxidative medicine and cellular longevity · 2022Article
- Activation of Pregnane X Receptor Sensitizes Mice to Hemorrhagic Shock-Induced Liver Injury.Hepatology (Baltimore, Md.) · 2019Article
- Endothelial Atg7 Deficiency Ameliorates Acute Cerebral Injury Induced by Ischemia/Reperfusion.Frontiers in neurology · 2018Article
- Plasma biomarkers to study mechanisms of liver injury in patients with hypoxic hepatitis.Liver international : official journal of the International Association for the Study of the Liver · 2017Article
- Article
- Apelin protect against multiple organ injury following hemorrhagic shock and decrease the inflammatory response.International journal of applied & basic medical researchArticle
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia-inducible factor-1 α (HIF-1 α ) and NF- κ B play important roles in the inflammatory response after hemorrhagic shock and resuscitation (H/R). Here, the role of myeloid HIF-1 α in liver hypoxia, injury, and inflammation after H/R with special regard to NF- κ B activation was studied.
methodsMice with a conditional HIF-1 α knockout (KO) in myeloid cell-line and wild-type (WT) controls were hemorrhaged for 90 min (30 ± 2 mm Hg) and resuscitated. Controls underwent only surgical procedures.
resultsAfter six hours, H/R enhanced the expression of HIF-1 α -induced genes vascular endothelial growth factor (VEGF) and adrenomedullin (ADM). In KO mice, this was not observed. H/R-induced liver injury in HIF-1 α KO was comparable to WT. Elevated plasma interleukin-6 (IL-6) levels after H/R were not reduced by HIF-1 α KO. Local hepatic hypoxia was not significantly reduced in HIF-1 α KO compared to controls after H/R. H/R-induced NF- κB phosphorylation in liver did not significantly differ between WT and KO.
conclusionsHere, deleting HIF-1 α in myeloid cells and thereby in Kupffer cells was not protective after H/R. This data indicates that other factors, such as NF- κB, due to its upregulated phosphorylation in WT and KO mice, contrary to HIF-1 α, are rather key modulators of inflammation after H/R in our model.
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