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Peer-reviewedCC BYSmart medicine

Cold-Inducible RNA-Binding Protein Alleviates Hypertensive Renal Injury Through the KEAP1-NRF2 Pathway.

  • Yue Zhang1
  • Qilin Li1
  • Man Luo2
  • Dongxu Hua1
  • Yanhui Sheng3,4
  • Lei Wang5
  • Peng Li1,6,7
7 affiliations
  1. 1Department of Cardiology The First Affiliated Hospital with Nanjing Medical University Nanjing China.
  2. 2Department of Emergency The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University Huai'an China.
  3. 3Department of Cardiology The Affiliated Suzhou Hospital with Nanjing Medical University Suzhou Municipal Hospital Gusu School of Nanjing Medical University Suzhou China.
  4. 4Jiangsu Province Hospital Nanjing China.
  5. 5Department of Rehabilitation Medicine School of Acupuncture-Moxibustion and Tuina and School of Health Preservation and Rehabilitation Nanjing University of Chinese Medicine Nanjing China.
  6. 6Department of Cardiology Shengli Clinical Medical College of Fujian Medical University Fujian Provincial Hospital Fuzhou University Affiliated Provincial Hospital Fuzhou China.
  7. 7Fujian Provincial Key Laboratory of Cardiovascular Disease Fujian Cardiovascular Institute Fujian Clinical Medical Research Center for Cardiovascular Diseases Fuzhou China.
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Abstract

Angiotensin II (Ang II) plays crucial roles in renal dysfunction, fibrotic changes, apoptosis, and oxidative stress. CIRBP, a cold-inducible RNA-binding protein, functions to maintain cellular homeostasis. However, its role in renal damage elicited by Ang II remains unclear. Here, we investigated the mechanisms through which Cirbp overexpression alleviates renal damage caused by Ang II, and Cirbp deletion induces basal renal injury. Transcriptomic analysis identified the involvement of Cirbp in hypertension-related renal injury. Across the animal and cell models, Cirbp overexpression attenuated Ang II-induced renal dysfunction, fibrosis, apoptosis, and inflammation, whereas Cirbp deficiency aggravated basal injury and increased renal susceptibility to injury. CIRBP activated the KEAP1-NRF2 antioxidant pathway to mitigate redox stress. This renoprotective effect was reversed following the application of the NRF2 inhibitor ML385, but was resumed by the NRF2 agonist RA839. Together, CIRBP modulates redox imbalance during Ang II-mediated renal damage through KEAP1-NRF2 signaling.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026coldinducible,
  title = {{Cold-Inducible RNA-Binding Protein Alleviates Hypertensive Renal Injury Through the KEAP1-NRF2 Pathway.}},
  author = {Yue Zhang and Qilin Li and Man Luo and Dongxu Hua and Yanhui Sheng and Lei Wang and Peng Li},
  journal = {Smart medicine},
  year = {2026},
  month = nov,
  doi = {10.1002/smmd.70062},
  url = {https://europepmc.org/article/MED/42999923},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Cold-Inducible RNA-Binding Protein Alleviates Hypertensive Renal Injury Through the KEAP1-NRF2 Pathway.
AU  - Yue Zhang
AU  - Qilin Li
AU  - Man Luo
AU  - Dongxu Hua
AU  - Yanhui Sheng
AU  - Lei Wang
AU  - Peng Li
PY  - 2026
DA  - 2026/11/07
JO  - Smart medicine
DO  - 10.1002/smmd.70062
UR  - https://europepmc.org/article/MED/42999923
AB  - Angiotensin II (Ang II) plays crucial roles in renal dysfunction, fibrotic changes, apoptosis, and oxidative stress. CIRBP, a cold-inducible RNA-binding protein, functions to maintain cellular homeostasis. However, its role in renal damage elicited by Ang II remains unclear. Here, we investigated the mechanisms through which Cirbp overexpression alleviates renal damage caused by Ang II, and Cirbp deletion induces basal renal injury. Transcriptomic analysis identified the involvement of Cirbp in hypertension-related renal injury. Across the animal and cell models, Cirbp overexpression attenuated Ang II-induced renal dysfunction, fibrosis, apoptosis, and inflammation, whereas Cirbp deficiency aggravated basal injury and increased renal susceptibility to injury. CIRBP activated the KEAP1-NRF2 antioxidant pathway to mitigate redox stress. This renoprotective effect was reversed following the application of the NRF2 inhibitor ML385, but was resumed by the NRF2 agonist RA839. Together, CIRBP modulates redox imbalance during Ang II-mediated renal damage through KEAP1-NRF2 signaling.
SN  - 2751-1863
SN  - 2751-1871
ER  -