ReviewFrontiers in medicine2021
The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI.
Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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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.
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Who cites it
52 citing papers in PubMed, 70 citations in OpenAlex.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Arginase 2 deficiency mitigates sepsis-associated acute kidney injury by alleviating lipid accumulation.Clinical and translational medicine · 2026Article
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Epigenetics-mediated pathological alterations and their diagnostic and therapeutic potential in sepsis-associated acute kidney injury.Clinical epigenetics · 2026Review
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Predictive value of monocyte-to-high-density lipoprotein cholesterol ratio for acute kidney injury following coronary artery bypass grafting.BMC cardiovascular disorders · 2026Article
- The Herbal PairFood science & nutrition · 2026Article
- Cell therapy strategies for organ regeneration.BMC medicine · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- BMAL1 regulates tubular epithelial-derived exosomal miR-27a-3p to inhibit macrophage-myofibroblast transition and alleviate ischemia/reperfusion-induced renal fibrosis.Theranostics · 2026Article
- NTN1 regulates autophagy through the MAP1B/DAPK1 axis to ameliorate acute kidney injuryOpen medicine (Warsaw, Poland) · 2026Article
- Shenlian (SL) Decoction Treat Diabetic Nephropathy by Regulating M1 Polarization of Macrophages and Pyroptosis of Renal Tubular Epithelial Cells.Journal of diabetes research · 2026Article
- Recent advances in PANoptosis research in kidney disease: mechanistic networks, pathological roles, and potential intervention strategies.Frontiers in immunology · 2026Review
- Sennoside A alleviates sepsis-triggered acute kidney injury via activating SIRT1 signaling pathway.Journal of molecular histology · 2025Article
- Study on the regulation of renal tubular cell apoptosis by SIRT1/NF-κB signaling pathway in septic acute kidney injury.Renal failure · 2025Article
- METTL1 aggravates sepsis-acute kidney injury by promoting mHistology and histopathology · 2025Article
- March6 Protects Against Acute Kidney Injury by Suppressing Renal Tubular Epithelial Cell Ferroptosis Through the Destabilization of P53 and ACSL4 Proteins.Inflammation · 2025Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Research advances on the role of programmed endothelial cell death in sepsis.Cell death discovery · 2025Review
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a systemic inflammatory response syndrome caused by infection, following with acute injury to multiple organs. Sepsis-induced acute kidney injury (AKI) is currently recognized as one of the most severe complications related to sepsis. The pathophysiology of sepsis-AKI involves multiple cell types, including macrophages, vascular endothelial cells (ECs) and renal tubular epithelial cells (TECs), etc. More significantly, programmed cell death including apoptosis, necroptosis and pyroptosis could be triggered by sepsis in these types of cells, which enhances AKI progress. Moreover, the cross-talk and connections between these cells and cell death are critical for better understanding the pathophysiological basis of sepsis-AKI. Mitochondria dysfunction and oxidative stress are traditionally considered as the leading triggers of programmed cell death. Recent findings also highlight that autophagy, mitochondria quality control and epigenetic modification, which interact with programmed cell death, participate in the damage process in sepsis-AKI. The insightful understanding of the programmed cell death in sepsis-AKI could facilitate the development of effective treatment, as well as preventive methods.
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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.