The Diagnostic and Therapeutic Potential of Galectin-3 in Cardiovascular Diseases

Sygitowicz, Grażyna; Maciejak-Jastrzębska, Agata; Sitkiewicz, Dariusz

doi:10.3390/biom12010046

Cited by 40 publications

(31 citation statements)

References 147 publications

(192 reference statements)

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“…Pathogenesis and poor outcomes of a variety of cardiovascular diseases, including HF, have been associated with the elevated level of plasma galectin-3. 19,35 Moreover, galectin-3 also plays a role in regulating immunity and inflammation. 36 Aldosterone induces the expression of galectin-3, which ultimately promotes tissue fibrosis, inflammation, and organ damage, including HF development.…”

Section: Discussionmentioning

confidence: 99%

Plasma Galectin-3 and H-FABP correlate with poor physical performance in patients with congestive heart failure

Ahmad

Karim

Khan

et al. 2023

Exp Biol Med (Maywood)

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Heart failure (HF) is often associated with compromised physical capacity in patients. However, it is unclear if established HF markers correlate with the physical performance of patients with congestive HF (CHF). We assessed the left ventricular end-systolic dimension (LVESD) and ejection fraction (LVEF) and, physical performance parameters, including short physical performance battery (SPPB), gait speed (GS), and handgrip strength (HGS) in 80 patients with CHF along with 59 healthy controls. Furthermore, levels of plasma HF markers galectin-3 and heart-specific fatty acid binding protein (H-FABP) were measured in relation to the severity of HF and physical performance. Irrespective of etiology, significantly greater LVESD and lower LVEF were observed in HF patients versus controls. As expected, the levels of HF markers galectin-3 and H-FABP were upregulated in the CHF patients which were accompanied by significantly elevated levels of plasma zonulin and inflammatory marker C-reactive protein (CRP). The SPPB scores, GS, and HGS were significantly lower in the ischemic and non-ischemic HF patients than controls. The level of galectin-3 was inversely correlated with SPPB scores ( r2 = 0.089, P = 0.01) and HGS ( r2 = 0.078, P = 0.01). Similarly, H-FABP levels were also inversely correlated with SPPB scores ( r2 = 0.06, P = 0.03) and HGS ( r2 = 0.109, P = 0.004) in the patients with CHF. Taken together, CHF adversely affects physical performance, and galectin-3 and H-FABP may serve as biomarkers of physical disability in patients with CHF. The robust correlations of galectin-3 and H-FABP with the physical performance parameters and CRP in CHF patients suggest that the poor physical performance may partly be caused due to systemic inflammation.

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Section: Discussionmentioning

confidence: 99%

Plasma Galectin-3 and H-FABP correlate with poor physical performance in patients with congestive heart failure

Ahmad

Karim

Khan

et al. 2023

Exp Biol Med (Maywood)

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“…В последние годы изучается возможность потенцирования этого эффекта путем направленного воздействия на ключевые механизмы патологического накопления коллагена и изменения его композиции в интерстиции, а также ведется поиск возможных терапевтических мишеней (галектин-3, матриксные металлопротеиназы, тканевый ингибитор матриксных металлопротеиназ 1, фактор дифференцировки роста-15, остеопонтин и др.) [148][149][150][151][152][153][154][155][156][157] Коррекция провоспалительного статуса Существенное значение патологии иммунной системы в механизмах ХСН является хорошо доказанным фактом [158][159][160][161]. В качестве перспективных мишеней терапии, направленной на снижение выраженности провоспалительных сдвигов на системном и локальном уровне, а также готовности кардиомиоцитов к реализации программ апоптоза, пироптоза и аутофагии, чаще всего обозначают Toll-подобные рецепторы, инфламмасомы (включая NODподобные рецепторы), цитокины, а также апоптотические и пироптотические эффекторные механизмы [162][163][164][165][166][167][168][169][170][171][172][173].…”

Section: лечебные подходыunclassified

Promising directions in the treatment of chronic heart failure: improving old or developing new ones?

et al. 2022

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Unprecedented advances of recent decades in clinical pharmacology, cardiac surgery, arrhythmology, and cardiac pacing have significantly improved the prognosis in patients with chronic heart failure (CHF). However, unfortunately, heart failure continues to be associated with high mortality. The solution to this problem consists in simultaneous comprehensive use in clinical practice of all relevant capabilities of continuously improving methods of heart failure treatment proven to be effective in randomized controlled trials (especially when confirmed by the results of studies in real clinical practice), on the one hand, and in development and implementation of innovative approaches to CHF treatment, on the other hand. This is especially relevant for CHF patients with mildly reduced and preserved left ventricular ejection fraction, as poor evidence base for the possibility of improving the prognosis in such patients cannot justify inaction and leaving them without hope of a clinical improvement in their condition. The lecture consistently covers the general principles of CHF treatment and a set of measures aimed at inotropic stimulation and unloading (neurohormonal, volumetric, hemodynamic, and immune) of the heart and outlines some promising areas of disease-modifying therapy.

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“…Galectin-3 contributes to various pathophysiological processes, including inflammation and fibrosis, cancer cell proliferation, adhesion, angiogenesis, cell migration, T-lymphocytes apoptosis and macrophage differentiation into infiltrative forms that stabilize tumor environments and polarization of tumor-associated macrophages [ 3 , 4 , 5 , 6 , 7 , 8 ]. Because of its disease-specific overexpression, human Gal-3 (hGal-3) has been proposed to be a therapeutic target and a biomarker of different pathological conditions including cancer and cardiovascular diseases [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Selectively Modified Lactose and N-Acetyllactosamine Analogs at Three Key Positions to Afford Effective Galectin-3 Ligands

Abdullayev

Kadav

Bandyopadhyay

et al. 2023

IJMS

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Galectins constitute a family of galactose-binding lectins overly expressed in the tumor microenvironment as well as in innate and adaptive immune cells, in inflammatory diseases. Lactose ((β-D-galactopyranosyl)-(1→4)-β-D-glucopyranose, Lac) and N-Acetyllactosamine (2-acetamido-2-deoxy-4-O-β-D-galactopyranosyl-D-glucopyranose, LacNAc) have been widely exploited as ligands for a wide range of galectins, sometimes with modest selectivity. Even though several chemical modifications at single positions of the sugar rings have been applied to these ligands, very few examples combined the simultaneous modifications at key positions known to increase both affinity and selectivity. We report herein combined modifications at the anomeric position, C-2, and O-3′ of each of the two sugars, resulting in a 3′-O-sulfated LacNAc analog having a Kd of 14.7 µM against human Gal-3 as measured by isothermal titration calorimetry (ITC). This represents a six-fold increase in affinity when compared to methyl β-D-lactoside having a Kd of 91 µM. The three best compounds contained sulfate groups at the O-3′ position of the galactoside moieties, which were perfectly in line with the observed highly cationic character of the human Gal-3 binding site shown by the co-crystal of one of the best candidates of the LacNAc series.

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The Diagnostic and Therapeutic Potential of Galectin-3 in Cardiovascular Diseases

Cited by 40 publications

References 147 publications

Plasma Galectin-3 and H-FABP correlate with poor physical performance in patients with congestive heart failure

Plasma Galectin-3 and H-FABP correlate with poor physical performance in patients with congestive heart failure

Promising directions in the treatment of chronic heart failure: improving old or developing new ones?

Selectively Modified Lactose and N-Acetyllactosamine Analogs at Three Key Positions to Afford Effective Galectin-3 Ligands

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