ArticleJournal of the American Society of Nephrology : JASN2015
Specific macrophage subtypes influence the progression of rhabdomyolysis-induced kidney injury.
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 95 papers.
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Who cites it
95 citing papers in PubMed, 153 citations in OpenAlex.
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- The Link between Alcohol Consumption and Kidney Injury.The American journal of pathology · 2026Review
- The temporal gene expression landscape of rhabdomyolysis-induced acute kidney injury reveals the timing of complement activation.Communications biology · 2025Article
- Voclosporin Overdose-Induced Peroxisomal Structural Changes and AKI Are Prevented by Renal Indole Detoxifier, INMT.Journal of the American Society of Nephrology : JASN · 2025Article
- Zileuton Attenuates Acute Kidney Injury in Glycerol-Induced Rhabdomyolysis by Regulating Myeloid-Derived Suppressor Cells in Mice.International journal of molecular sciences · 2025Article
- The efficiency of blood cell counts and inflammatory indices in prediction of need for acute kidney injury in patients with crush syndrome.BMC nephrology · 2025Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Curcumin-copper complex nanoparticles as antioxidant nanozymes for acute kidney injury alleviation.Materials today. Bio · 2025Article
- PRDM16 suppresses pyroptosis to attenuate the progression of AKI caused by rhabdomyolysis via upregulation of USP10.Cellular and molecular life sciences : CMLS · 2025Article
- An adoptive cell therapy with TREM2-overexpressing macrophages mitigates the transition from acute kidney injury to chronic kidney disease.Clinical and translational medicine · 2025Article
- EZH2-mediated macrophage-to-myofibroblast transition contributes to calcium oxalate crystal-induced kidney fibrosis.Communications biology · 2025Article
- A Newly Identified Protective Role of C5a Receptor 1 in Kidney Tubules against Toxin-Induced Acute Kidney Injury.The American journal of pathology · 2025Article
- Rhabdomyolysis, Acute Kidney Injury, and Mortality in Ebola Virus Disease: Retrospective Analysis of Cases From the Eastern Democratic Republic of the Congo, 2019.The Journal of infectious diseases · 2024Article
- The novel potential therapeutic target PSMP/MSMP promotes acute kidney injury via CCR2.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024Review
- Astragalus Polysaccharide Mitigates Rhabdomyolysis-Induced Acute Kidney Injury via Inhibition of M1 Macrophage Polarization and the cGAS-STING Pathway.Journal of inflammation research · 2024Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyolysis can be life threatening if complicated by AKI. Macrophage infiltration has been observed in rat kidneys after glycerol-induced rhabdomyolysis, but the role of macrophages in rhabdomyolysis-induced AKI remains unknown. Here, in a patient diagnosed with rhabdomyolysis, we detected substantial macrophage infiltration in the kidney. In a mouse model of rhabdomyolysis-induced AKI, diverse renal macrophage phenotypes were observed depending on the stage of the disease. Two days after rhabdomyolysis, F4/80(low)CD11b(high)Ly6b(high)CD206(low) kidney macrophages were dominant, whereas by day 8, F4/80(high)CD11b(+)Ly6b(low)CD206(high) cells became the most abundant. Single-cell gene expression analyses of FACS-sorted macrophages revealed that these subpopulations were heterogeneous and that individual cells simultaneously expressed both M1 and M2 markers. Liposomal clodronate-mediated macrophage depletion significantly reduced the early infiltration of F4/80(low)CD11b(high)Ly6b(high)CD206(low) macrophages. Furthermore, transcriptionally regulated targets potentially involved in disease progression, including fibronectin, collagen III, and chemoattractants that were identified via single-cell analysis, were verified as macrophage-dependent in situ. In vitro, myoglobin treatment induced proximal tubular cells to secrete chemoattractants and macrophages to express proinflammatory markers. At day 30, liposomal clodronate-mediated macrophage depletion reduced fibrosis and improved both kidney repair and mouse survival. Seven months after rhabdomyolysis, histologic lesions were still present but were substantially reduced with prior depletion of macrophages. These results suggest an important role for macrophages in rhabdomyolysis-induced AKI progression and advocate the utility of long-term follow-up for patients with this disease.
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