ArticleInternational journal of molecular sciences2020
Macrophage-Derived Iron-Bound Lipocalin-2 Correlates with Renal Recovery Markers Following Sepsis-Induced Kidney Damage.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Study of the relationship between iron metabolism disorders and sepsis-associated liver injury: A prospective observational study.World journal of gastroenterology · 2025Observational
- Lipocalin-2 and intestinal diseases.World journal of gastroenterology · 2024Review
- Regulation of renal ischemia-reperfusion injury and tubular epithelial cell ferroptosis by pparγ m6a methylation: mechanisms and therapeutic implications.Biology direct · 2024Article
- Identification of key genes as potential diagnostic biomarkers in sepsis by bioinformatics analysis.PeerJ · 2024Article
- Protective effect of omega-3 polyunsaturated fatty acids on sepsis via the AMPK/mTOR pathway.Pharmaceutical biology · 2023Article
- Article
- Extracellular status of thrombospondin-2 in type 2 diabetes mellitus and utility as a biomarker in the determination of early diabetic kidney disease.BMC nephrology · 2023Article
- LCN2 secreted by tissue-infiltrating neutrophils induces the ferroptosis and wasting of adipose and muscle tissues in lung cancer cachexia.Journal of hematology & oncology · 2023Article
- Bibliometric and visualization analysis of kidney repair associated with acute kidney injury from 2002 to 2022.Frontiers in pharmacology · 2023Article
- Binding to Iron Quercetin Complexes Increases the Antioxidant Capacity of the Major Birch Pollen Allergen Bet v 1 and Reduces Its Allergenicity.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- A Mixture of Pure, Isolated Polyphenols Worsens the Insulin Resistance and Induces Kidney and Liver Fibrosis Markers in Diet-Induced Obese Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2022Article
- Serum Lipocalin-2 Levels Are Increased and Independently Associated With Early-Stage Renal Damage and Carotid Atherosclerotic Plaque in Patients With T2DM.Frontiers in endocrinology · 2022Article
- Iron-Deficiency in Atopic Diseases: Innate Immune Priming by Allergens and Siderophores.Frontiers in allergy · 2022Review
- Tumor cell-imposed iron restriction drives immunosuppressive polarization of tumor-associated macrophages.Journal of translational medicine · 2021Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Major signaling pathways and key mediators of macrophages in acute kidney injury (Review).Molecular medicine reports · 2021Review
- Iron-Bound Lipocalin-2 Protects Renal Cell Carcinoma from Ferroptosis.Metabolites · 2021Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
During the course of sepsis in critically ill patients, kidney dysfunction and damage are among the first events of a complex scenario toward multi-organ failure and patient death. Acute kidney injury triggers the release of lipocalin-2 (Lcn-2), which is involved in both renal injury and recovery. Taking into account that Lcn-2 binds and transports iron with high affinity, we aimed at clarifying if Lcn-2 fulfills different biological functions according to its iron-loading status and its cellular source during sepsis-induced kidney failure. We assessed Lcn-2 levels both in serum and in the supernatant of short-term cultured renal macrophages (MΦ) as well as renal tubular epithelial cells (TEC) isolated from either Sham-operated or cecal ligation and puncture (CLP)-treated septic mice. Total kidney iron content was analyzed by Perls' staining, while Lcn-2-bound iron in the supernatants of short-term cultured cells was determined by atomic absorption spectroscopy. Lcn-2 protein in serum was rapidly up-regulated at 6 h after sepsis induction and subsequently increased up to 48 h. Lcn-2-levels in the supernatant of TEC peaked at 24 h and were low at 48 h with no change in its iron-loading. In contrast, in renal MΦ Lcn-2 was low at 24 h, but increased at 48 h, where it mainly appeared in its iron-bound form. Whereas TEC-secreted, iron-free Lcn-2 was associated with renal injury, increased MΦ-released iron-bound Lcn-2 was linked to renal recovery. Therefore, we hypothesized that both the cellular source of Lcn-2 as well as its iron-load crucially adds to its biological function during sepsis-induced renal injury.
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