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Acrolein produced during acute kidney injury promotes tubular cell death

Seishi Aihara1, Kumiko Torisu2, Yutaro Hirashima1

  • 1Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Biochemical and Biophysical Research Communications
|May 15, 2023
PubMed

Insights

Toxic acrolein, produced from polyamines during cell damage, worsens acute kidney injury (AKI) by causing tubular cell death. Controlling acrolein levels may offer a new therapeutic strategy for kidney ischemia-reperfusion injury.

Area of Science:

  • Nephrology
  • Cellular Biology
  • Toxicology

Background:

  • Acute kidney injury (AKI) presents a significant global health challenge with high morbidity and mortality rates.
  • Polyamines are crucial for cellular functions, but their breakdown product, acrolein, can be toxic.
  • Spermine oxidase (SMOX) is an enzyme responsible for producing acrolein from polyamines during cellular damage.

Purpose of the Study:

  • To investigate the role of acrolein in exacerbating AKI through renal tubular cell death.
  • To explore the therapeutic potential of targeting acrolein accumulation in ischemia-reperfusion injury.

Main Methods:

  • Utilized a mouse model of renal ischemia-reperfusion injury and human proximal tubule cells (HK-2).
  • Quantified acrolein levels using acroleinRED and assessed SMOX expression.
  • Investigated the effects of acrolein and its scavenger cysteamine on cell death and fibrosis markers (TGFB1).
  • Examined mitochondrial membrane potential and employed siRNA-mediated knockdown of SMOX.

Main Results:

  • Acrolein levels were elevated in ischemia-reperfusion injured kidneys and in HK-2 cells undergoing hypoxia-reoxygenation.
  • Acrolein exposure induced cell death and increased TGFB1 mRNA expression in HK-2 cells.
  • Cysteamine treatment reduced acrolein-induced TGFB1 upregulation, preserved mitochondrial membrane potential, and decreased cell death.
  • SMOX knockdown mitigated hypoxia-reoxygenation-induced acrolein accumulation and cell death.

Conclusions:

  • Acrolein significantly contributes to renal tubular cell death and exacerbates AKI during ischemia-reperfusion injury.
  • Targeting acrolein accumulation, potentially via scavengers like cysteamine, represents a promising therapeutic avenue for AKI.
Keywords:
AcroleinAcute kidney injuryIschemia-reperfusion injuryPolyamineRenal tubular cellSpermine oxidase

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