ArticleScientific reports2019
Impact of aging on transition of acute kidney injury to chronic kidney disease.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Markers of the ageing macrophage: a systematic review and meta-analysis.Frontiers in immunology · 2023Pooled it
- Teprasiran, a Small Interfering RNA, for the Prevention of Acute Kidney Injury in High-Risk Patients Undergoing Cardiac Surgery: A Randomized Clinical Study.Circulation · 2021Trial
- Apelin-13 Pretreatment Attenuates Age-Associated Renal Fibrotic Remodeling Following I/R Injury.Biomedicines · 2026Article
- Therapeutic silicate biomaterials for sarcopenia treatment by inhibiting inflammation and enhancing muscle regeneration through regulation of Sarcolipin/SIRT signaling pathway.Bioactive materials · 2025Article
- The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.International journal of biological sciences · 2025Review
- Targeting cellular senescence in kidney diseases and aging: A focus on mesenchymal stem cells and their paracrine factors.Cell communication and signaling : CCS · 2024Review
- Injury-induced Foxm1 expression in the mouse kidney drives epithelial proliferation by a cyclin F-dependent mechanism.JCI insight · 2024Article
- Targeted Drug Therapy for Senescent Cells Alleviates Unilateral Ureteral Obstruction-Induced Renal Injury in Rats.Pharmaceutics · 2024Article
- SGLT2i improves kidney senescence by down-regulating the expression of LTBP2 in SAMP8 mice.Journal of cellular and molecular medicine · 2024Article
- Free heme and hemopexin in acute kidney injury after cardiopulmonary bypass and transient renal ischemia.Clinical and translational science · 2023Article
- Molecular Mechanisms Associated with Aging Kidneys and Future Perspectives.International journal of molecular sciences · 2023Review
- Roles of interferon regulatory factor 4 in the AKI-CKD transition, glomerular diseases and kidney allograft rejection.Renal failure · 2023Review
- Altered gut microbiome plays an important role in AKI to CKD transition in aged mice.Frontiers in medicine · 2023Article
- Bibliometric and visualization analysis of kidney repair associated with acute kidney injury from 2002 to 2022.Frontiers in pharmacology · 2023Article
- Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- Characteristics, risk factors and outcomes of community-acquired acute kidney injury in the elderly: a prospective tertiary hospital study, Egypt.African health sciences · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022Review
- Roles of SIRT6 in kidney disease: a novel therapeutic target.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) increases the risk of end stage renal disease among the elderly, but the precise underlying mechanism is unknown. We investigated the effects of aging on AKI-to-chronic kidney disease (CKD) transition, focusing on renal inflammation. Aged and young C57BL/6 mice were subjected to bilateral ischemia-reperfusion injury (IRI). Baseline proinflammatory cytokine levels of kidneys were elevated in aged mice. After IRI, aged mice also showed persistent M1 dominant inflammation, with increased proinflammatory cytokines during the recovery phase. Persistent M1 inflammation was associated with blunted activation of CSF-1/IRF4 signal for M1/M2 polarization, but in vitro macrophage polarization with cytokine stimulation was not different between young and aged mononuclear cells. The tubular expressions of cell cycle arrest markers increased in aged mice during recovery phase, and in vitro transwell experiments showed that mononuclear cells or M1 macrophages co-cultured with arrested proximal tubular cells at G1 phase significantly impaired M2 polarization, suggesting that prolonged G1 arrest might be involved in persistent M1 inflammation in aged mice. Finally, M1 dominant inflammation in aged mice resulted in fibrosis progression. Our data show that impaired M2 polarization partially driven by senescent tubule cells with cell-cycle arrest may lead to an accelerated progression to CKD in the elderly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.