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Acute Kidney Injury I: Introduction01:22

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Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...
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Sema3dhi Fibroblasts Promote Acute Kidney Injury Fibrotic Progression Through Confining Endothelial Cell Migration.

Qiuyu Xie1, Xiaohong Xin1, Weijian Yao1

  • 1Renal Division, Peking University Institute of Nephrology, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Peking University First Hospital, Xishiku Street #8, Beijing, 100034, China.

International Journal of Biological Sciences
|January 29, 2026
PubMed
Summary

Activated fibroblasts promote kidney fibrosis after acute kidney injury (AKI). Targeting Sema3d signaling in fibroblasts may prevent chronic kidney disease (CKD) progression and microvascular loss.

Keywords:
Sema3dacute kidney injuryangiogenesisendothelial cellfibroblastmigration

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Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Acute kidney injury (AKI) can lead to chronic kidney disease (CKD) characterized by fibrosis and microvascular rarefaction.
  • The role of activated fibroblasts in AKI-to-CKD transition and their direct impact on microvasculature remain incompletely understood.

Purpose of the Study:

  • To investigate the function of fibroblast subpopulations in AKI-CKD progression.
  • To elucidate the mechanism by which fibroblasts affect endothelial cells and microvasculature.
  • To identify potential therapeutic targets for mitigating renal fibrosis.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of a unilateral ischemia reperfusion injury (uIRI) mouse model to identify fibroblast subpopulations.
  • In vitro experiments using conditioned medium from specific fibroblast cells (Sema3dhi-NRK49F) on human umbilical vein endothelial cells (HUVECs).
  • In vivo studies involving systemic administration of Sema3d-shRNA via adeno-associated virus serotype 9 (AAV9) in mice.
  • Analysis of human scRNA-seq data and immunofluorescence staining of human kidney samples.

Main Results:

  • Five fibroblast subpopulations were identified, with C0-Sema3dhi fibroblasts increasing post-injury and correlating with reduced endothelial cells.
  • Conditioned medium from Sema3dhi fibroblasts inhibited endothelial cell migration and angiogenesis.
  • Sema3d secreted by these fibroblasts activates Plexin D1 on endothelial cells, leading to cytoskeletal changes and suppressed function.
  • Sema3d-shRNA treatment reduced Sema3d levels and alleviated renal fibrosis in mice.
  • SEMA3D+ fibroblasts were found in human kidney disease samples.

Conclusions:

  • Sema3dhi fibroblasts contribute to microvascular dysfunction and renal fibrosis in AKI-CKD progression.
  • The Sema3d/Plexin D1 signaling pathway is a key mechanism mediating fibroblast-endothelial cell interactions.
  • Targeting the Sema3d pathway presents a promising therapeutic strategy to prevent fibrosis and preserve renal function after AKI.