ArticlePhysiological reports2018
Persistent expression of neutrophil gelatinase-associated lipocalin and M2 macrophage markers and chronic fibrosis after acute kidney injury.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
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- Apelin-13 exerts protective effects against acute kidney injury by lysosomal function regulation.Renal failure · 2025Article
- The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.Cellular & molecular biology letters · 2025Review
- The role of autophagy in fibrosis: Mechanisms, progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Monocytes and Macrophages in Kidney Disease and Homeostasis.International journal of molecular sciences · 2024Review
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- Young Plasma Attenuated Chronic Kidney Disease Progression after Acute Kidney Injury by Inhibiting Inflammation in Mice.Aging and disease · 2023Article
- Twist1 regulates macrophage plasticity to promote renal fibrosis through galectin-3.Cellular and molecular life sciences : CMLS · 2022Article
- Doxycycline Alters the Porcine Renal Proteome and Degradome during Hypothermic Machine Perfusion.Current issues in molecular biology · 2022Article
- Article
- Urinary biomarkers as point-of-care tests for predicting progressive deterioration of kidney function in congenital anomalies of kidney and urinary tract: trefoil family factors (TFFs) as the emerging biomarkers.Pediatric nephrology (Berlin, Germany) · 2021Article
- Methylation in pericytes after acute injury promotes chronic kidney disease.The Journal of clinical investigation · 2020Article
- Sepsis-Associated Acute Kidney Disease.Kidney international reports · 2020Article
- "Point of no return" in unilateral renal ischemia reperfusion injury in mice.Journal of biomedical science · 2020Article
- M2 macrophages predict worse long-term outcomes in human acute tubular necrosis.Scientific reports · 2020Article
- Macrophage polarization in chronic kidney disease: a balancing act between renal recovery and decline?American journal of physiology. Renal physiology · 2019Review
- Targeted VEGF (Vascular Endothelial Growth Factor) Therapy Induces Long-Term Renal Recovery in Chronic Kidney Disease via Macrophage Polarization.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Macrophages: versatile players in renal inflammation and fibrosis.Nature reviews. Nephrology · 2019Review
- Persistent expression of neutrophil gelatinase-associated lipocalin and M2 macrophage markers and chronic fibrosis after acute kidney injury.Physiological reports · 2018Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent epidemiologic studies revealed a correlation between acute kidney injury (AKI) episodes and the progression to chronic kidney disease (CKD). Although the severity and duration of the initial insult likely predict the development of CKD, information regarding tissue markers predictive of early development of renal fibrosis is limited. We investigated key markers in fibrotic kidney in rats and mice. Seven- to eight-week-old male Sprague-Dawley rats underwent bilateral ischemia-reperfusion injury (IRI). Kidney tissues were collected to determine the markers correlated with the severity of kidney fibrosis. In a separate set, a specific chemokine (C-C motif) receptor 2 (CCR2) inhibitor, RS-102895, was administered to 9-week-old male C57BL/6J mice that underwent unilateral IRI (9.2 mg/kg/day in drinking water for 17 days) to investigate whether blockade of the monocyte chemotactic protein-1 (MCP-1) signaling was sufficient to prevent fibrosis. Among candidate tissue markers, neutrophil gelatinase-associated lipocalin (NGAL) and MCP-1 mRNA expressions were correlated with kidney fibrosis. Studies on macrophage polarity showed that mRNA expression of M2, but not M1 macrophage markers, were correlated with acute-phase serum creatinine and fibrosis. Pharmacological blockade of the MCP-1-CCR2 signaling downregulated CCR2, which was insufficient to improve fibrosis in mouse unilateral IRI model, suggesting that additional, redundant pathways contribute to fibrosis. These findings suggested that tissue NGAL expression and M2 macrophage markers are promising markers that show severity of kidney fibrosis. Mechanistic involvement of these markers in CKD pathogenesis warrant additional investigation.
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