
| 10.3390/ijms22041514
http://scihub22266oqcxt.onion/10.3390/ijms22041514
 33546372!7913498!33546372
free
free
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Int+J+Mol+Sci 2021 ; 22 (4): � Nephropedia Template TP
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Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models #MMPMID33546372Yachie AInt J Mol Sci 2021[Feb]; 22 (4): � 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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