ReviewNature reviews. Nephrology2022
Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury.
Review in Nature reviews. Nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.
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Who cites it
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- The global prevalence of acute kidney injury (AKI) in preterm neonates: an epidemiological meta-analysis.European journal of pediatrics · 2026Pooled it
- Lactate in acute kidney injury: pathobiology, risk stratification, and clinical interpretation.Renal failure · 2026Review
- Development and validation of prediction models for any and severe acute kidney injury in children with sepsis.Pediatric nephrology (Berlin, Germany) · 2026Article
- Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Association of the Endothelial Activation and Stress Index (EASIX) with Clinical Outcomes in Patients with Pneumosepsis: A Retrospective Cohort Study.Life (Basel, Switzerland) · 2026Article
- Staphylococcus aureus-vascular endothelium interactions: Mechanisms and therapeutic opportunities.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Article
- Epigenetics-mediated pathological alterations and their diagnostic and therapeutic potential in sepsis-associated acute kidney injury.Clinical epigenetics · 2026Review
- An interpretable prediction model for severe sepsis-associated acute kidney injury in older ICU patients with sepsis: a prospective multicenter cohort study.BMC geriatrics · 2026Article
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Predictive value of monocyte-to-high-density lipoprotein cholesterol ratio for acute kidney injury following coronary artery bypass grafting.BMC cardiovascular disorders · 2026Article
- Immunoinflammatory biomarkers for sepsis-associated acute kidney injury: a multicenter prospective cohort study.Immunity & ageing : I & A · 2026Article
- PAFAH2 deficiency drives sepsis-induced vascular leakage by promoting ECHS1-mediated suppression of protein crotonylation and mitochondrial dysfunction.Inflammation and regeneration · 2026Article
- Pseudogene-Derived Long Noncoding RNAs GSTM3P1/Gstm2-ps1 Exacerbate Sepsis-Associated Acute Kidney Injury by Suppressing Their Parent Gene Translation.The American journal of pathology · 2026Article
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Investigating the roles of macrophage age and circulating extracellular vesicles in cytoprotection of hypoxic renal tubular cell stress.BMC molecular and cell biology · 2026Article
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Microbial and Host Inflammatory Factors Induce Permeability and Activate Cytokine Production by Human Glomerular Microvascular Endothelial Cells.Shock (Augusta, Ga.) · 2026Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microvascular endothelial cells in the kidney have been a neglected cell type in sepsis-induced acute kidney injury (sepsis-AKI) research; yet, they offer tremendous potential as pharmacological targets. As endothelial cells in distinct cortical microvascular segments are highly heterogeneous, this Review focuses on endothelial cells in their anatomical niche. In animal models of sepsis-AKI, reduced glomerular blood flow has been attributed to inhibition of endothelial nitric oxide synthase activation in arterioles and glomeruli, whereas decreased cortex peritubular capillary perfusion is associated with epithelial redox stress. Elevated systemic levels of vascular endothelial growth factor, reduced levels of circulating sphingosine 1-phosphate and loss of components of the glycocalyx from glomerular endothelial cells lead to increased microvascular permeability. Although coagulation disbalance occurs in all microvascular segments, the molecules involved differ between segments. Induction of the expression of adhesion molecules and leukocyte recruitment also occurs in a heterogeneous manner. Evidence of similar endothelial cell responses has been found in kidney and blood samples from patients with sepsis. Comprehensive studies are needed to investigate the relationships between segment-specific changes in the microvasculature and kidney function loss in sepsis-AKI. The application of omics technologies to kidney tissues from animals and patients will be key in identifying these relationships and in developing novel therapeutics for sepsis.
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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.