ArticleAmerican journal of physiology. Renal physiology2012
Renal cortical hemopexin accumulation in response to acute kidney injury.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 42 citations in OpenAlex.
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- Is Hemopexin a Nephrotoxin or a Marker of Kidney Injury in Renal Ischemia-Reperfusion?Biomolecules · 2024Article
- Identification of common molecular signatures of SARS-CoV-2 infection and its influence on acute kidney injury and chronic kidney disease.Frontiers in immunology · 2023Article
- Urinary Protein Profiling for Potential Biomarkers of Chronic Kidney Disease: A Pilot Study.Diagnostics (Basel, Switzerland) · 2022Article
- Identifying Candidate Protein Markers of Acute Kidney Injury in Acute Decompensated Heart Failure.International journal of molecular sciences · 2022Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Biomarkers Associated with Organ-Specific Involvement in Juvenile Systemic Lupus Erythematosus.International journal of molecular sciences · 2021Review
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- The Acute Phase Response Is a Prominent Renal Proteome Change in Sepsis in Mice.International journal of molecular sciences · 2019Article
- Mechanisms of haemolysis-induced kidney injury.Nature reviews. Nephrology · 2019Review
- Distinct patterns of transcriptional and epigenetic alterations characterize acute and chronic kidney injury.Scientific reports · 2018Article
- Role of TLR4 signaling in the nephrotoxicity of heme and heme proteins.American journal of physiology. Renal physiology · 2018Article
- Genotypic and phenotypic characterization of G6PD deficiency in Bengali adults with severe and uncomplicated malaria.Malaria journal · 2017Observational
- Combined iron sucrose and protoporphyrin treatment protects against ischemic and toxin-mediated acute renal failure.Kidney international · 2016Article
- Targeting Iron Homeostasis in Acute Kidney Injury.Seminars in nephrology · 2016Review
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- Marked protection against acute renal and hepatic injury after nitrited myoglobin + tin protoporphyrin administration.Translational research : the journal of laboratory and clinical medicine · 2015Article
- Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation.Archives of toxicology · 2015Article
- Acute hepatic ischemic-reperfusion injury induces a renal cortical "stress response," renal "cytoresistance," and an endotoxin hyperresponsive state.American journal of physiology. Renal physiology · 2014Article
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3 authors at 2 institutions in 1 country.
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Abstract
Hemopexin (Hpx) is a liver-generated acute phase reactant that binds and neutralizes prooxidant free heme. This study tested whether acute kidney injury (AKI) triggers renal Hpx accumulation, potentially impacting heme Fe-mediated tubular injury. Mice were subjected to glycerol, cisplatin, ischemia-reperfusion (I/R), or endotoxemic [lipopolysaccharide (LPS)] AKI. In each instance, 3- to 30-fold renal cortical and isolated proximal tubule segment (PTS) Hpx increases resulted. Although renal cortex and PTS showed variable Hpx mRNA increases, due, in part, to increased mRNA stability, mRNA levels did not correlate with renal Hpx protein accumulation. Conversely, AKI evoked three- to fourfold increases in hepatic Hpx gene induction, which corresponded with three- to fourfold plasma Hpx increases. Renal immunohistochemistry, and increased urinary Hpx excretion, indicated that circulating Hpx gains tubule luminal/urinary access, followed by proximal tubule endocytic uptake. Paradoxically, in cultured renal cells (HK-2, HEK-293), Fe depletion, and not free heme excess, increased Hpx mRNA. LPS acutely increased HK-2 cell Hpx mRNA. This finding, coupled with observations that LPS evoked ∼30-fold greater renal Hpx mRNA increases than any other AKI model, suggests that inflammation, not heme exposure, activates the renal Hpx gene. Each form of AKI evoked early increases in circulating free heme, which subsequently fell to subnormal levels as plasma Hpx rose. In addition, purified Hpx blunted free Fe-mediated HK-2 cell death. In sum, these data indicated that AKI-associated hepatic stress generates Hpx, which gains renal tubule access. Given its ability to bind free heme and mitigate free Fe toxicity, Hpx loading can potentially confer cytoprotective effects.
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