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Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway

Kunyu Shen1, Jinhua Miao1, Qiongdan Gao1

  • 1Division of Nephrology, Nanfang Hospital, Southern Medical University; National Clinical Research Center for Kidney Disease; State Key Laboratory of Organ Failure Research; Guangdong Provincial Institute of Nephrology; Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou, 510515, China.

Cell Death Discovery
|October 28, 2022
PubMed

Insights

Annexin A2 (ANXA2) protects against acute kidney injury (AKI) by enhancing autophagy and lysosomal function. This protein modulates the β-catenin/TFEB pathway, offering new therapeutic potential for AKI treatment.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Acute kidney injury (AKI) poses a global health challenge with limited therapeutic options.
  • Improving autophagy and lysosomal function shows promise in mitigating AKI.
  • Identifying key modulators of these cellular processes is crucial for developing new AKI treatments.

Purpose of the Study:

  • To investigate the role of Annexin A2 (ANXA2) in the context of AKI.
  • To elucidate the underlying molecular mechanisms by which ANXA2 influences kidney injury, autophagy, and lysosomal function.
  • To explore ANXA2 as a potential therapeutic target for AKI.

Main Methods:

  • Utilized a cisplatin-induced AKI mouse model.
  • Assessed ANXA2 expression levels in renal tubules.
  • Manipulated ANXA2 expression (ectopic expression and knockdown) to evaluate its effects on kidney injury, apoptosis, lysosomal function, and autophagic flux.
  • Performed transcriptome sequencing to identify involved signaling pathways.
  • Conducted in vitro experiments to confirm the ANXA2-mediated signaling cascade involving β-catenin and transcription factor EB (TFEB).

Main Results:

  • ANXA2 expression was upregulated in renal tubules following cisplatin-induced AKI.
  • Ectopic ANXA2 expression ameliorated kidney injury by improving lysosomal function and enhancing autophagic flux, reducing tubular cell apoptosis.
  • ANXA2 knockdown exacerbated AKI progression by impairing lysosomal function and autophagy.
  • Transcriptome analysis implicated the β-catenin signaling pathway.
  • In vitro studies confirmed that ANXA2 activates β-catenin, leading to TFEB activation, which promotes lysosome biogenesis and boosts autophagic flux, ultimately alleviating AKI.

Conclusions:

  • Annexin A2 (ANXA2) plays a protective role against acute kidney injury.
  • ANXA2 enhances autophagy and lysosomal function, thereby mitigating kidney damage.
  • The protective mechanism involves the activation of the β-catenin/TFEB signaling pathway, highlighting ANXA2 as a promising therapeutic target for AKI.

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