Galectin-3 in Cardiorenal Syndrome: A Systematic Review and Meta-analysis
Yujia Zhou, Yaobin Liang, Zonglin Shen, Zhubin Lun, Jiancong Zhou, Xindan Cao, Peiwen Li, Jianfeng YeAbstract
Background
Galectin-3 (Gal-3) regulates cell adhesion, apoptosis, inflammation, and immune activation. Recent studies on Gal-3 and renocardiac or cardiorenal syndrome (CRS) show conflicting results. This meta-analysis systematically evaluated Gal-3 in predicting CRS subtypes and mortality.
Methods
We searched PubMed, EMBASE, The Cochrane Library, Web of Science, and the China National Knowledge Infrastructure (CNKI) for papers investigating the relationship between serum Gal-3 levels and CRS, from database inception to July 10, 2025, with an updated search conducted on March 1, 2026. Observational studies evaluating Gal-3 in relation to CRS incidence and mortality, heart failure (HF) mortality, and chronic kidney disease (CKD) mortality were included.
Results
A total of 281 articles were retrieved, and 22 were ultimately included after screening. High Gal-3 levels significantly predicted incident HF in CKD patients (hazard ratios [HR]: 1.19; 95% confidence interval [CI]: 1.10-1.28; P<0.0001) and predicted all-cause mortality in CKD patients (HR: 2.45; 95% CI: 1.37-4.37; P=0.002). In HF patients, Elevated Gal-3 levels were associated with a higher risk of the occurrence of CRS (odds ratios [OR]: 1.12; 95% CI: 1.03-1.22; P=0.01) and also predicted all-cause mortality (HR: 1.55; 95% CI: 1.33-1.82; P<0.00001). Finally, the 2 included studies indicated that Gal-3 was significantly associated with all-cause mortality in CRS patients.
Conclusions
Gal-3 may serve as a significant predictor for the incidence of Type 2 and Type 4 CRS, the risk of mortality in HF and CKD patients, and all-cause mortality in CRS patients.