Galectin-3: A Modifiable Risk Factor in Heart Failure

Abstract

Myocardial galectin-3 is upregulated upon cardiac stressors such as angiotensin II and pressure overload leading to cardiac remodeling and heart failure. The expression level of galectin-3 mirrors the progression and severity of heart failure and therefore, galectin-3 is being used as a biomarker for heart failure. However, as galectin-3 is causally involved in pathological myocardial fibrosis it has been suggested that galectin-3 also actively contributes to heart failure development. In this review we discuss how galectin-3 could be a target for therapy in heart failure. Currently, attempts are being made to target or inhibit galectin-3 using natural or pharmaceutical inhibitors with the aim to ameliorate heart failure. Available experimental evidence suggests that galectin-3 inhibition indeed may represent a novel tool to treat heart failure. A strong interaction with aldosterone, another strong pro-fibrotic factor, has been described. Clinical studies are needed to prove if galectin-3 may be used to install specific treatment regimens.

Galectin-3 and post-myocardial infarction cardiac remodeling

“…Galectin-3 was an independent predictor for LVEF after 4 months. Elevated levels were correlated with a significant lower LVEF (van der Velde et al, 2014). Further clinical data are scarce and suggest a potential relationship between galectin-3 levels and higher risk of HF development after MI.…”

“…Clinically, MRAs improve survival in patients with symptomatic chronic HF after MI (Maisel et al, 2014;Pitt et al, 2003). Recently, it was shown that MRAs reverse cardiac and renal expression of galectin-3 in hypertensive rats (Calvier et al, 2015).…”

Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis

“…Despite its role as a biomarker that mirrors the progression and severity of heart failure, 53 galectin-3 does not play a crucial role in the pathogenesis of the fibrotic cardiomyopathy associated with pressure overload. Useful and reliable biomarkers of cardiac remodeling do not necessarily serve a key biological function, but they may be released after stress, reflecting another injurious process.…”

New possibilities of diagnostics and control of efficacy of drug therapy for chronic heart failure

“…Однако, кроме напряжения стенки миокарда, в патогенезе ХСН также принимают участие и другие про-цессы, такие как воспаление и фиброз. Натрийуретические пептиды не дают возможности оценивать выраженность данных процессов, в связи с чем поиск биомаркеров фиброза и воспаления является актуальным.В исследованиях DEAL-HF и СOACH была продемон-стрирована способность нового биомаркера галектина-3 отражать процессы воспаления и фиброза, лежащих в осно-ве ремоделирования миокарда у пациентов с ХСН [1][2][3].Галектин-3 принадлежит к семейству β-галактозид-связывающих протеинов. Благодаря наличию в своей Гямджян К. А., Кукес В. Г. p=0.02).…”

“…В исследованиях DEAL-HF и СOACH была продемон-стрирована способность нового биомаркера галектина-3 отражать процессы воспаления и фиброза, лежащих в осно-ве ремоделирования миокарда у пациентов с ХСН [1][2][3].…”