ArticleeLife2022
Pericyte-mediated constriction of renal capillaries evokes no-reflow and kidney injury following ischaemia.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Endothelial Cell-Pericyte Crosstalk in the Brain Balances Microvascular Stability and Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Article
- Functional targeting of PTTG1 in pericytes restores vascular integrity in diabetic retina.Science advances · 2026Article
- Peri-Microvascular Glycogen and Lactate Regulate Capillary Constrictions and Ischemia Outcome in Mice.Journal of neurochemistry · 2026Article
- Article
- GLP-1 activates KNature communications · 2026Article
- The role of the vascular niche in regulating kidney tubulointerstitial fibrosis.Kidney international · 2026Review
- Research progress of nanoparticles in the diagnosis and treatment of renal ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Review
- Effect of metformin on the autophagy process in renal ischemia reperfusion injury.Journal of molecular histology · 2026Article
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- Leucine-rich α-2-glycoprotein 1 initiates the onset of diabetic retinopathy in mice.Science translational medicine · 2025Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Lipocalin-2 Restores Soluble Guanylyl Cyclase-Dependent Dilation of the Afferent Arteriole After Renal Transplantation or Ex Vivo Hypoxia/Reoxygenation in Mice.Acta physiologica (Oxford, England) · 2025Article
- Advances in Pathophysiology and Novel Therapeutic Strategies for Coronary No-Reflow Phenomenon.Biomedicines · 2025Review
- Pericyte and Endothelial Cell Responses within Murine Cerebral Capillaries After Blood Flow Cessation.bioRxiv : the preprint server for biology · 2025Article
- Impact of NA-1 on Pericyte-Driven Vasoconstriction and Its Role in No-Reflow During Cerebral Ischemia-Reperfusion.CNS neuroscience & therapeutics · 2025Article
- Deficiency of fibroblast growth factor 2 promotes contractile phenotype of pericytes in ascending thoracic aortic aneurysm.American journal of physiology. Heart and circulatory physiology · 2025Article
- Pericytes in the brain and heart: functional roles and response to ischaemia and reperfusion.Cardiovascular research · 2025Review
- Metabolic and Microcirculatory Changes in Severe Renal Ischemia-Reperfusion and Ischemic Preconditioning in the Rat: Are They Detectable in the First Hour of Reperfusion?Life (Basel, Switzerland) · 2025Article
- Molecular mechanisms and therapeutic advances of peritubular capillary neogenesis in acute kidney injury.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute kidney injury is common, with ~13 million cases and 1.7 million deaths/year worldwide. A major cause is renal ischaemia, typically following cardiac surgery, renal transplant or severe haemorrhage. We examined the cause of the sustained reduction in renal blood flow ('no-reflow'), which exacerbates kidney injury even after an initial cause of compromised blood supply is removed. Adult male Sprague-Dawley rats, or NG2-dsRed male mice were used in this study. After 60 min kidney ischaemia and 30-60 min reperfusion, renal blood flow remained reduced, especially in the medulla, and kidney tubule damage was detected as Kim-1 expression. Constriction of the medullary descending vasa recta and cortical peritubular capillaries occurred near pericyte somata, and led to capillary blockages, yet glomerular arterioles and perfusion were unaffected, implying that the long-lasting decrease of renal blood flow contributing to kidney damage was generated by pericytes. Blocking Rho kinase to decrease pericyte contractility from the start of reperfusion increased the post-ischaemic diameter of the descending vasa recta capillaries at pericytes, reduced the percentage of capillaries that remained blocked, increased medullary blood flow and reduced kidney injury. Thus, post-ischaemic renal no-reflow, contributing to acute kidney injury, reflects pericytes constricting the descending vasa recta and peritubular capillaries. Pericytes are therefore an important therapeutic target for treating acute kidney injury.
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