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CIAPIN1 improves sepsis-induced acute kidney injury by inhibiting mitochondrial damage

Jingcong Huang1, Minyu Shi1, Ziqing Zhang1

  • 1Department of Emergency Medicine, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China.

Pathology, Research and Practice
|February 19, 2026
PubMed

Insights

This study reveals the cytokine-induced apoptosis inhibitor 1 (CIAPIN1)-optic atrophy 1 (OPA1) pathway as a key regulator in sepsis-associated acute kidney injury (SA-AKI). It highlights their role in mitigating kidney damage by improving mitochondrial function and reducing inflammation.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Sepsis-associated acute kidney injury (SA-AKI) is a significant cause of mortality in sepsis patients, yet its underlying pathological mechanisms are not fully understood.
  • Identifying novel therapeutic targets requires a deeper understanding of the molecular pathways involved in SA-AKI pathogenesis.

Purpose of the Study:

  • To investigate the regulatory role of the cytokine-induced apoptosis inhibitor 1 (CIAPIN1)-optic atrophy 1 (OPA1) signaling axis in SA-AKI.
  • To elucidate the mechanisms by which this axis influences cellular apoptosis, mitochondrial damage, and inflammation in the context of SA-AKI.

Main Methods:

  • Utilized lipopolysaccharide (LPS)-stimulated HK-2 cells for in vitro loss- and gain-of-function experiments to assess CIAPIN1 and OPA1 roles.
  • Investigated the functional interaction between CIAPIN1 and OPA1, and examined N6-methyladenosine (m6A) modification's impact on CIAPIN1 expression.
  • Established a murine AKI model induced by cecal ligation and puncture for in vivo evaluation of Ciapin1 silencing effects.

Main Results:

  • CIAPIN1 overexpression in LPS-stimulated HK-2 cells reduced apoptosis, improved mitochondrial membrane potential, restored mitochondrial protein expression, and suppressed inflammatory factor release.
  • OPA1 overexpression counteracted the detrimental effects of CIAPIN1 knockdown on apoptosis, mitochondrial dysfunction, and inflammation in HK-2 cells.
  • Ciapin1 knockdown in a murine AKI model exacerbated renal injury, apoptosis, mitochondrial damage, and inflammation; WTAP was identified to promote m6A modification of CIAPIN1 mRNA.

Conclusions:

  • The CIAPIN1-OPA1 signaling axis represents a novel mechanistic basis for SA-AKI.
  • This pathway plays a critical role in regulating mitochondrial function, inflammatory responses, and cellular apoptosis in renal tissues during septic stress.
  • Targeting the CIAPIN1-OPA1 axis may offer a potential therapeutic strategy for mitigating SA-AKI.
Keywords:
CIAPIN1M6AMitochondrial dysfunctionOPA1Sepsis-associated acute kidney injury

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