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Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling

Jiaxiao Li1, Chen Wu1, Yuqi Zhu1

  • 1Department of Nephrology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 5, 2026
PubMed

Insights

Annexin A13 (ANXA13) protects the kidneys from acute kidney injury (AKI). Lower ANXA13 levels in AKI patients suggest it could be a novel therapeutic target for kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Acute kidney injury (AKI) is a significant risk factor for chronic kidney disease.
  • The molecular mechanisms underlying AKI pathogenesis are not fully understood.
  • Current treatment options for AKI are limited.

Purpose of the Study:

  • To investigate the role of Annexin A13 (ANXA13) in the context of AKI.
  • To elucidate the renoprotective mechanisms of ANXA13.
  • To explore ANXA13 as a potential therapeutic target for AKI.

Main Methods:

  • Clinical analysis of ANXA13 levels in AKI patients and mouse models.
  • Functional studies involving ANXA13 overexpression and silencing in vivo and in vitro.
  • Investigation of ANXA13 interaction with TGF-β receptor type 1 and Smad3 signaling pathways.
  • Analysis using renal tubule epithelial cell-specific Anxa13 knockout mice and Smad3 Knockout mice.

Main Results:

  • ANXA13 expression is reduced in kidneys of AKI patients and mouse models.
  • ANXA13 overexpression confers protection against AKI, while silencing exacerbates injury.
  • ANXA13 directly inhibits TGF-β receptor type 1 phosphorylation, inactivating Smad3 signaling.
  • Smad3 signaling negatively regulates ANXA13 transcription via binding to its 3'UTR.

Conclusions:

  • ANXA13 exhibits significant renoprotective effects in AKI.
  • The renoprotection is mediated by the inhibition of TGF-β/Smad3 signaling pathway.
  • ANXA13 represents a promising novel therapeutic agent for AKI.
Keywords:
AKIANXA13TGF‐β receptor type 1TGF‐β/Smad3

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