Dear editor,We read with great interest the article entitled "Short and Long-Term Prognostic Significance of Galectin-3 in Patients with ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention" by Köktürk et al. 1 We congratulate the authors and would like to discuss some points about the relationship between Galectin-3 and cardiovascular disease (CVD).Patients with ST-Elevation Myocardial Infarction (STEMI) were divided into high and low galectin-3 groups for comparison. 1 They found that the primary clinical outcomes including cardiovascular (CV) mortality, non-fatal reinfarction, stroke, and target vessel revascularization were significantly higher in the high galectin-3 group. They also found that galectin-3 was associated with adverse CVevents, heart failure (HF), and re-hospitalization.Interestingly, Asleh et al. 2 found that elevated galectin-3 was associated with increased risk of death and HF in patients with acute myocardial infarction (AMI). Li et al. 3 showed that galectin-3 was an independent risk factor for major adverse cardiac events (MACEs) in acute coronary syndrome (ACS) patients. Moreover, one study also showed that galectin-3 predicted the composite of CV death and HF hospitalization at 1 year in STEMI patients. 4 These studies are consistent with the conclusions made by Köktürk et al. 1 The mechanisms by which galectin-3 participates in CVD and affects prognosis remain unclear. Galectin-3, a proinflammatory cytokine, is mainly secreted by activated macrophages. 5 It has been proven to play an important role in many physiological and pathological processes such as cell adhesion, apoptosis, inflammation, which is involved in the formation of atherosclerosis. 5 Furthermore, it is recognized that galectin-3 has an adverse effect on cardiac remodeling and myofibroblast activation. 6,7 However, several studies have suggested cardioprotective effect of galectin-3. In a C57BL/6 galectin-3 knockout mice model, gene deletion of galectin-3 reduced the lifespan and markedly increased age-dependent mechanisms of myocardial hypertrophy, apoptosis, and fibrosis. 8 In a mouse model of myocardial infarction (MI), galectin-3 knockout displayed an increased trend towards mortality, chiefly due to ventricular rupture, emphasizing that galectin-3 is necessary for normal wound healing, especially during the initial phases of cardiac repair. 9In conclusion, galectin-3 plays a role in CVD, but its relevance and specific mechanism remain controversial. More research is required to further clarify the role of galectin-3 in the CV system.