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Updated: Apr 16, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

695

Sepsis-associated AKI: epithelial cell dysfunction

David R Emlet1, Andrew D Shaw2, John A Kellum1

  • 1Center for Critical Care Nephrology, University of Pittsburgh, Pittsburgh, PA; Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.

Seminars in Nephrology
|March 22, 2015
PubMed

Insights

Sepsis-induced acute kidney injury (AKI) in critically ill patients has high mortality. This review explores how renal tubule epithelial cell (RTEC) dysfunction contributes to sepsis-AKI, impacting patient outcomes and kidney health.

Area of Science:

  • Nephrology
  • Critical Care Medicine
  • Immunology

Background:

  • Sepsis-induced acute kidney injury (AKI) is a common and lethal complication in critically ill patients.
  • AKI in sepsis survivors often leads to chronic kidney disease, highlighting the need for effective therapies.
  • Current therapeutic strategies for sepsis-AKI are limited, necessitating a deeper understanding of its underlying mechanisms.

Purpose of the Study:

  • To elucidate the cellular and molecular etiologies of sepsis-induced AKI.
  • To review the multifaceted origins of AKI, including inflammatory and immune responses, microvascular dysfunction, and metabolic alterations.
  • To discuss the critical role of renal tubule epithelial cells (RTECs) in the pathogenesis of sepsis-AKI.

Main Methods:

  • Literature review of cellular and molecular mechanisms of sepsis-induced AKI.
  • Analysis of current hypotheses regarding RTEC dysfunction in sepsis-AKI.
  • Synthesis of data on damage-associated molecular patterns (DAMPs), pathogen-associated molecular patterns (PAMPs), and immune activation in AKI.

Main Results:

  • Sepsis-AKI involves complex interactions including DAMPs, PAMPs, inflammation, immune activation, and microvascular disturbances.
  • Oxidative stress, bioenergetic alterations, and cell-cycle dysregulation significantly impact RTECs.
  • Cellular de-differentiation and re-differentiation processes in RTECs are key determinants of kidney injury and recovery.

Conclusions:

  • Renal tubule epithelial cells (RTECs) are central effectors in sepsis-induced AKI, mediating diverse cellular insults.
  • Understanding RTEC fate determination is crucial for developing novel therapeutic interventions for sepsis-AKI.
  • Further research into RTEC responses to sepsis is essential for improving patient survival and long-term kidney function.
Keywords:
DAMPs and PAMPsSepsisacute kidney injuryrenal tubule epithelial cell

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