ArticleExperimental and therapeutic medicine2019
Biological effects of autophagy in mice with sepsis-induced acute kidney injury.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 23 citations in OpenAlex.
- Sinapic Acid Attenuates LPS-Induced Acute Kidney Injury in Rats: Changes in Autophagy-Related, Apoptotic, Inflammatory, and Oxidative Stress Markers.Journal of biochemical and molecular toxicology · 2026Article
- Review
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Diagnostic PANoptosis-related genes in acute kidney injury: bioinformatics, machine learning, and validation.Annals of medicine · 2025Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Ergosterol Protects Canine MDCK Cells from Gentamicin-Induced Damage by Modulating Autophagy and Apoptosis.Metabolites · 2025Article
- The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review.Drug design, development and therapy · 2025Review
- Sigma-1 Receptor Rescues Autophagy Through AMPK/mTOR Signaling Pathway in Sepsis-Induced Acute Kidney Injury.International journal of general medicine · 2025Article
- Sepsis-Associated Acute Kidney Injury: Where Are We Now?Medicina (Kaunas, Lithuania) · 2024Review
- The role of inflammatory response and metabolic reprogramming in sepsis-associated acute kidney injury: mechanistic insights and therapeutic potential.Frontiers in immunology · 2024Review
- miR-506-3p induces autophagy of renal tubular epithelial cells in sepsis through targeting PI3K pathway.Aging · 2023Article
- Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection.Frontiers in immunology · 2023Review
- Sepsis-induced AKI: From pathogenesis to therapeutic approaches.Frontiers in pharmacology · 2022Review
- Programmed Cell Death in Sepsis Associated Acute Kidney Injury.Frontiers in medicine · 2022Review
- miR-181a-5p Inhibits Pyroptosis in Sepsis-Induced Acute Kidney Injury through Downregulation of NEK7.Journal of immunology research · 2022Article
- miR‑214 ameliorates sepsis‑induced acute kidney injury via PTEN/AKT/mTOR‑regulated autophagy.Molecular medicine reports · 2021Article
- SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation.Cell death & disease · 2021Article
- Downregulation of IRF2 Alleviates Sepsis-Related Acute Kidney Injury in vitro and in vivo.Drug design, development and therapy · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated whether autophagy is activated after sepsis-induced acute kidney injury (AKI) and explored its biological role. Seventy-two normal C57 mice were randomly divided into sham operation group, cecal ligation and puncture (CLP) group and CLP+3-MA (autophagy inhibitor) group; 24 mice in each group. Mice in CLP and CLP+3-MA group were treated with cecal ligation to establish sepsis, while mice in sham operation group were treated with the same surgical operations, but not cecal ligation. Blood samples were collected from 12 mice of each group and the levels of serum creatinine (Cr) and blood urea nitrogen (BUN) were measured. The pathological changes were observed. The remaining 12 mice in each group were kept and the survival rate was recorded. Changes in the expressions of autophagy-related proteins were detected by reverse transcription-semi-quantitative PCR and western blotting. The results revealed that the levels of Cr and BUN in CLP and CLP+3-MA group were significantly higher than those in sham operation group (P<0.05), and the levels of Cr and BUN in CLP+3-MA group were higher than those in CLP group (P<0.05). The pathological score of renal injury in CLP+3-MA group was significantly higher than that of CLP group (P<0.01). The expression levels of Beclin1 and LC3-II/I were significantly increased in CLP group compared to sham operation group (P<0.01), while the expression of p62 was decreased (P<0.01). After 3-MA treatment the expression levels of Beclin1 and LC3-II/I were decreased, compared with CLP group, but accumulation of p62 occurred, and the degree of renal injury was increased. In conclusion, AKI induced by sepsis in mice can induce apoptosis and activate autophagy. The activation of autophagy aggravates the renal injury in mice, which in turn inhibits AKI after sepsis.
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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 Socratic graph.