Int J Mol Med. 2026 Aug;58(2):210. doi: 10.3892/ijmm.2026.5881. Epub 2026 Jun 5.
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.
PMID:42246189 | DOI:10.3892/ijmm.2026.5881