ArticleAmerican journal of physiology. Renal physiology2024
Myeloid-specific ferritin light chain deletion does not exacerbate sepsis-associated AKI.
Article in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting macrophage ferritin heavy chain mitigates ferroptosis and lung injury in experimental acute respiratory distress syndrome.Nature communications · 2026Article
- SUMOylation protects against sepsis-associated acute kidney injury by stabilizing IκBα.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Biomarkers as Beacons: Illuminating Sepsis-Associated Hepato-Renal Injury.International journal of molecular sciences · 2025Review
- Mechanistic study on electroacupuncture-regulated circadian autophagy for inhibiting ferroptosis in hippocampal neurons and alleviating depression-like behaviors in adulthood induced by early chronic sleep deprivation.Frontiers in neurology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Sepsis-associated acute kidney injury (SA-AKI) is a key contributor to the life-threatening sequelae attributed to sepsis. Mechanistically, SA-AKI is a consequence of unabated myeloid cell activation and oxidative stress that induces tubular injury. Iron mediates inflammatory pathways directly and through regulating the expression of myeloid-derived ferritin, an iron storage protein comprising ferritin light (FtL) and ferritin heavy chain (FtH) subunits. Previous work revealed that myeloid FtH deletion leads to a compensatory increase in intracellular and circulating FtL and is associated with amelioration of SA-AKI. We designed this study to test the hypothesis that loss of myeloid FtL and subsequently, circulating FtL will exacerbate the sepsis-induced inflammatory response and worsen SA-AKI. We generated a novel myeloid-specific FtL knockout mouse (FtL
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Registered trials
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