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10.3390/ijms22041514

http://scihub22266oqcxt.onion/10.3390/ijms22041514
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33546372!7913498!33546372
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suck abstract from ncbi


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pmid33546372      Int+J+Mol+Sci 2021 ; 22 (4): ä
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  • Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models #MMPMID33546372
  • Yachie A
  • Int J Mol Sci 2021[Feb]; 22 (4): ä PMID33546372show ga
  • Since Yachie et al. reported the first description of human heme oxygenase (HO)-1 deficiency more than 20 years ago, few additional human cases have been reported in the literature. A detailed analysis of the first human case of HO-1 deficiency revealed that HO-1 is involved in the protection of multiple tissues and organs from oxidative stress and excessive inflammatory reactions, through the release of multiple molecules with anti-oxidative stress and anti-inflammatory functions. HO-1 production is induced in vivo within selected cell types, including renal tubular epithelium, hepatic Kupffer cells, vascular endothelium, and monocytes/macrophages, suggesting that HO-1 plays critical roles in these cells. In vivo and in vitro studies have indicated that impaired HO-1 production results in progressive monocyte dysfunction, unregulated macrophage activation and endothelial cell dysfunction, leading to catastrophic systemic inflammatory response syndrome. Data from reported human cases of HO-1 deficiency and numerous studies using animal models suggest that HO-1 plays critical roles in various clinical settings involving excessive oxidative stress and inflammation. In this regard, therapy to induce HO-1 production by pharmacological intervention represents a promising novel strategy to control inflammatory diseases.
  • |*Oxidative Stress[MESH]
  • |Anemia, Hemolytic/*metabolism[MESH]
  • |Animals[MESH]
  • |Growth Disorders/*metabolism[MESH]
  • |Heme Oxygenase-1/*deficiency/*metabolism[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]


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