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Peer-reviewedCC BYInternational Journal of Molecular Medicine

Experimental rodent models of cardiorenal syndrome types 3 and 4: Insights and clinical relevance (Review)

Abstract

Cardiorenal syndrome (CRS) encompasses the bidirectional and complex interaction between cardiac and renal dysfunction. The present review focuses on CRS types 3 and 4, highlighting the negative effects of acute kidney injury and chronic kidney disease, respectively, on cardiac function. The present review focuses on pathophysiological mechanisms, associating renal impairment with cardiovascular events, paying particular attention to systemic inflammation, oxidative stress, endothelial damage and neurohormonal activation. From fundamental science to clinical applications, the investigation of CRS remains a challenge. In this context, some experimental models mimicking CRS types 3 and 4 have been used, including 5/6 nephrectomy, unilateral ureteral obstruction, renal ischemia‑reperfusion and adenine‑ or cisplatin‑induced kidney injury. While these models are valuable for studying such disease mechanisms, their limitations in mimicking human pathophysiology are discussed, and their strengths and weaknesses are critically addressed. Advancing and refining preclinical models should be prioritized in future research to enhance clinical relevance and accelerate the development of targeted therapies for CRS.

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BibTeX
@article{figueroa2026experimental,
  title = {{Experimental rodent models of cardiorenal syndrome types 3 and 4: Insights and clinical relevance (Review)}},
  author = {Stefanny Figueroa and Siyi Huang and Javier Reyes Osorio and Jean-Jacques Boffa and Cristián Amador and Christos E Chadjichristos and Louis Boutin},
  journal = {International Journal of Molecular Medicine},
  year = {2026},
  month = jun,
  doi = {10.3892/ijmm.2026.5881},
  url = {https://hal.science/hal-05794582v1},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Experimental rodent models of cardiorenal syndrome types 3 and 4: Insights and clinical relevance (Review)
AU  - Stefanny Figueroa
AU  - Siyi Huang
AU  - Javier Reyes Osorio
AU  - Jean-Jacques Boffa
AU  - Cristián Amador
AU  - Christos E Chadjichristos
AU  - Louis Boutin
PY  - 2026
DA  - 2026/06/04
JO  - International Journal of Molecular Medicine
DO  - 10.3892/ijmm.2026.5881
UR  - https://hal.science/hal-05794582v1
AB  - Cardiorenal syndrome (CRS) encompasses the bidirectional and complex interaction between cardiac and renal dysfunction. The present review focuses on CRS types 3 and 4, highlighting the negative effects of acute kidney injury and chronic kidney disease, respectively, on cardiac function. The present review focuses on pathophysiological mechanisms, associating renal impairment with cardiovascular events, paying particular attention to systemic inflammation, oxidative stress, endothelial damage and neurohormonal activation. From fundamental science to clinical applications, the investigation of CRS remains a challenge. In this context, some experimental models mimicking CRS types 3 and 4 have been used, including 5/6 nephrectomy, unilateral ureteral obstruction, renal ischemia‑reperfusion and adenine‑ or cisplatin‑induced kidney injury. While these models are valuable for studying such disease mechanisms, their limitations in mimicking human pathophysiology are discussed, and their strengths and weaknesses are critically addressed. Advancing and refining preclinical models should be prioritized in future research to enhance clinical relevance and accelerate the development of targeted therapies for CRS.
SN  - 1107-3756
SN  - 1791-244X
ER  -