ReviewFrontiers in immunology2023
Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Renal-targeted tFNA-TPP nanoagonist treats acute kidney injury by amplifying mitophagy.Materials today. Bio · 2026Article
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.Histology and histopathology · 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
- To explore the molecular mechanism of IRF7 involved in acute kidney injury in sepsis based on proteomics.Proteome science · 2025Article
- Gaps in PLTP mechanism research in sepsis-associated acute kidney injury and improvement strategies based on new evidence.Critical care (London, England) · 2025Article
- INHIBITING SIRT2 ATTENUATES SEPSIS-INDUCED ACUTE KIDNEY INJURY VIA FOXO1 ACETYLATION-MEDIATED AUTOPHAGY ACTIVATION.Shock (Augusta, Ga.) · 2025Article
- The non-linear association between creatinine-to-albumin ratio and medium-term mortality in patients with sepsis accompanied by acute kidney injury in the intensive care unit: a retrospective study based on the MIMIC database and external validation.Frontiers in cellular and infection microbiology · 2025Article
- TM9SF1 as a Novel Prognostic Biomarker for Sepsis Severity and Mortality: A Longitudinal Study.Journal of inflammation research · 2025Article
- Sepsis-Associated Acute Kidney Injury: What's New Regarding Its Diagnostics and Therapeutics?Diagnostics (Basel, Switzerland) · 2024Review
- Dexmedetomidine alleviates intestinal ischemia/reperfusion injury by modulating intestinal neuron autophagy and mitochondrial homeostasis via Nupr1 regulation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- Sepsis-Associated Acute Kidney Injury: Where Are We Now?Medicina (Kaunas, Lithuania) · 2024Review
- Elevated Activated Partial Thromboplastin Time as a Predictor of 28-Day Mortality in Sepsis-Associated Acute Kidney Injury: A Retrospective Cohort Analysis.International journal of general medicine · 2024Article
- Tiliroside Protects against Lipopolysaccharide-Induced Acute Kidney Injury via Intrarenal Renin-Angiotensin System in Mice.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute kidney injury (SI-AKI), a common critically ill, represents one of the leading causes of global death. Emerging evidence reveals autophagy as a pivotal modulator of SI-AKI. Autophagy affects the cellular processes of renal lesions, including cell death, inflammation, and immune responses. Herein, we conducted a systematic and comprehensive review on the topic of the proposed roles of autophagy in SI-AKI. Forty-one relevant studies were finally included and further summarized and analyzed. This review revealed that a majority of included studies (24/41, 58.5%) showed an elevation of the autophagy level during SI-AKI, while 22% and 19.5% of the included studies reported an inhibition and an elevation at the early stage but a declination of renal autophagy in SI-AKI, respectively. Multiple intracellular signaling molecules and pathways targeting autophagy (e.g. mTOR, non-coding RNA, Sirtuins family, mitophagy, AMPK, ROS, NF-Kb, and Parkin) involved in the process of SI-AKI, exerting multiple biological effects on the kidney. Multiple treatment modalities (e.g. small molecule inhibitors, temsirolimus, rapamycin, polydatin, ascorbate, recombinant human erythropoietin, stem cells, Procyanidin B2, and dexmedetomidine) have been found to improve renal function, which may be attributed to the elevation of the autophagy level in SI-AKI. Though the exact roles of autophagy in SI-AKI have not been well elucidated, it may be implicated in preventing SI-AKI through various molecular pathways. Targeting the autophagy-associated proteins and pathways may hint towards a new prospective in the treatment of critically ill patients with SI-AKI, but more preclinical studies are still warranted to validate this hypothesis.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.