ArticleJournal of the American Society of Nephrology : JASN2015
Heme Oxygenase-1 Regulates Myeloid Cell Trafficking in AKI.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- Acute kidney injury results in long-term alterations of kidney lymphatics in mice.American journal of physiology. Renal physiology · 2024Article
- Single molecule array measures of LRRK2 kinase activity in serum link Parkinson's disease severity to peripheral inflammation.Molecular neurodegeneration · 2024Article
- The Role of Heme Oxygenase-1 as an Immunomodulator in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Identification of Cytoprotective Small-Molecule Inducers of Heme-Oxygenase-1.Antioxidants (Basel, Switzerland) · 2022Article
- Different Acute Kidney Injury Patterns after Renal Ischemia Reperfusion Injury and Extracorporeal Membrane Oxygenation in Mice.International journal of molecular sciences · 2022Article
- Adapting decarbonylation chemistry for the development of prodrugs capable ofChemical science · 2021Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Preexisting heart failure with reduced ejection fraction attenuates renal fibrosis after ischemia reperfusion via sympathetic activation.Scientific reports · 2021Article
- UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021Review
- Deciphering the Role of Heme Oxygenase-1 (HO-1) Expressing Macrophages in Renal Ischemia-Reperfusion Injury.Biomedicines · 2021Review
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
- Regulation of Complement Activation by Heme Oxygenase-1 (HO-1) in Kidney Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Chess Not Checkers: Complexities Within the Myeloid Response to the Acute Kidney Injury Syndrome.Frontiers in medicine · 2021Review
- Immunomodulatory Effects of Heme Oxygenase-1 in Kidney Disease.Frontiers in medicine · 2021Review
- New insights into the role of heme oxygenase-1 in acute kidney injury.Kidney research and clinical practice · 2020Review
- Dynamic signature of lymphangiogenesis during acute kidney injury and chronic kidney disease.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Renal Inflammation and Fibrosis: A Double-edged Sword.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury.Frontiers in immunology · 2019Article
- Pretreatment with Cholecalciferol Alleviates Renal Cellular Stress Response during Ischemia/Reperfusion-Induced Acute Kidney Injury.Oxidative medicine and cellular longevity · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Renal ischemia-reperfusion injury is mediated by a complex cascade of events, including the immune response, that occur secondary to injury to renal epithelial cells. We tested the hypothesis that heme oxygenase-1 (HO-1) expression, which is protective in ischemia-reperfusion injury, regulates trafficking of myeloid-derived immune cells in the kidney. Age-matched male wild-type (HO-1(+/+)), HO-1-knockout (HO-1(-/-)), and humanized HO-1-overexpressing (HBAC) mice underwent bilateral renal ischemia for 10 minutes. Ischemia-reperfusion injury resulted in significantly worse renal structure and function and increased mortality in HO-1(-/-) mice. In addition, there were more macrophages (CD45(+) CD11b(hi)F4/80(lo)) and neutrophils (CD45(+) CD11b(hi) MHCII(-) Gr-1(hi)) in HO-1(-/-) kidneys than in sham and HO-1(+/+) control kidneys subjected to ischemia-reperfusion. However, ischemic injury resulted in a significant decrease in the intrarenal resident dendritic cell (DC; CD45(+)MHCII(+)CD11b(lo)F4/80(hi)) population in HO-1(-/-) kidneys compared with controls. Syngeneic transplant experiments utilizing green fluorescent protein-positive HO-1(+/+) or HO-1(-/-) donor kidneys and green fluorescent protein-negative HO-1(+/+) recipients confirmed increased migration of the resident DC population from HO-1(-/-) donor kidneys, compared to HO-1(+/+) donor kidneys, to the peripheral lymphoid organs. This effect on renal DC migration was corroborated in myeloid-specific HO-1(-/-) mice subjected to bilateral ischemia. These mice also displayed impaired renal recovery and increased fibrosis at day 7 after injury. These results highlight an important role for HO-1 in orchestrating the trafficking of myeloid cells in AKI, which may represent a key pathway for therapeutic intervention.
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