The relationship between serum galectin-3 and serum markers of cardiac extracellular matrix turnover in heart failure patients

Lin, Yen‐Hung; Lin, Lian‐Yu; Wu, Yen‐Wen; Chien, Kuo–Liong; Lee, Chi-Ming; Hsu, Ron‐Bin; Chao, Chia-Lun; Wang, Shoei‐Shen; Hsein, Yenh-Chen; Liao, Lin-Chu; Ho, Yi‐Lwun; Chen, Ming-Fong

doi:10.1016/j.cca.2009.09.001

Cited by 139 publications

(111 citation statements)

References 26 publications

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“…In fact, since fibrosis is one of the main mechanisms underlying increased ventricular stiffness and diastolic dysfunction [23], the pro-fibrotic and immune-modulatory properties of galectin-3 have been claimed to explain the association between plasma levels of this lectin and the presence and severity of heart failure [24]. This interpretation is consistent with the finding that galectin-3 was significantly correlated with serum markers of cardiac ECM turnover in patients with heart failure [25].…”

Section: Introductionsupporting

confidence: 69%

Galectin-3 in diabetic patients

Pugliese

Iacobini

Ricci

et al. 2014

Clinical Chemistry and Laboratory Medicine (CCLM)

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Galectin-3 is a versatile molecule which exerts several and sometimes opposite functions in various pathophysiological processes. Recently, galectin-3 has gained attention as a powerful predictor of heart failure and mortality, thus becoming a useful prognostic marker in clinical practice. Moreover, though not specifically investigated in diabetic cohorts, plasma levels of galectin-3 correlated with the prevalence of diabetes and related metabolic conditions, thus suggesting that pharmacological blockade of this lectin might be successful for treating heart failure especially in subjects suffering from these disorders. Indeed, galectin-3 is considered not only as a marker of heart failure, but also as a mediator of the disease, due to its pro-fibrotic action, though evidence comes mainly from studies in galectin-3 deficient mice. However, these studies have provided contrasting results, with either attenuation or acceleration of organ fibrosis and inflammation, depending on the experimental setting and particularly on the levels of advanced glycation endproducts (AGEs)/advanced lipoxidation endproducts (ALEs), of which galectin-3 is a scavenging receptor. In fact, under conditions of increased AGE/ALE levels, galectin-3 ablation was associated with tissue-specific outcomes, reflecting the AGE/ALE-receptor function of this lectin. Conversely, in experimental models of acute inflammation and fibrosis, galectin-3 deficiency resulted in attenuation of tissue injury. There is a need for prospective studies in diabetic patients specifically investigating the relation of galectin-3 levels with complications and for further animal studies in order to establish the effective role of this lectin in organ damage before considering its pharmacological blockade in the clinical setting.

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Section: Introductionsupporting

confidence: 69%

Galectin-3 in diabetic patients

Pugliese

Iacobini

Ricci

et al. 2014

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…In a mouse model of desmin-deficient HF, knocking out the gene for osteopontin resulted in dramatically decreased galectin-3 expression and subsequently less cardiac fibrosis and improved echocardiographic parameters of ventricular function (3 ). In patients with chronic HF, galectin-3 concentrations have been correlated with markers of extracellular matrix turnover, such as type III amino-terminal propeptide of procol- lagen (PIIINP) and matrix metalloproteinase 2 (MMP-2), implying a relationship between macrophage activation and collagen turnover (18 ). Intriguingly, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a monocyte-derived antiinflammatory and antifibrotic peptide that is degraded by ACE, inhibits galectin-3 expression in the left ventricle and reduces galectin-3-induced macrophage activation and migration (19 ).…”

Section: Galectin-3 and The Pathobiology Of Hfmentioning

confidence: 99%

Galectin-3 and the Development of Heart Failure after Acute Coronary Syndrome: Pilot Experience from PROVE IT-TIMI 22

et al. 2012

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BACKGROUND Galectin-3 is a β-galactoside–binding lectin that has been implicated in cardiac fibrosis and remodeling, is increased in models of failure-prone hearts, and has prognostic value in patients with heart failure (HF). The relationship between galectin-3 and the development of HF after acute coronary syndrome (ACS) is unknown. METHODS In a nested case-control study among patients with ACS in PROVE IT-TIMI 22, we identified 100 cases with a hospitalization for new or worsening HF. Controls were matched (1:1) for age, sex, ACS type, and randomized treatment. Serum galectin-3 was measured at baseline (within 7 days post-ACS). RESULTS Patients who developed HF had higher baseline galectin-3 [median 16.7 μg/L (25th, 75th percentile 14.0, 20.6) vs 14.6 μg/L (12.0, 17.6), P = 0.004]. Patients with baseline galectin-3 above the median had an odds ratio of 2.1 (95% CI 1.2–3.6) for developing HF, P = 0.010. Galectin-3 showed a graded relationship with risk of HF. Cases were more likely to have hypertension, diabetes, prior MI, and prior HF; after adjustment for these factors, this graded relationship with galectin-3 quartile and HF remained significant [adjusted OR 1.4 (95% CI 1.1–1.9), P = 0.020]. When BNP was added to the model, the relationship between galectin-3 and HF was attenuated [adjusted OR 1.3 (95% CI: 0.96–1.9), P = 0.08]. CONCLUSIONS The finding that galectin-3 is associated with the risk of developing HF following ACS adds to emerging evidence supporting galectin-3 as a biomarker of adverse remodeling contributing to HF as well as a potential therapeutic target.

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“…Moreover, in the study by Lin et al [34], it was confirmed that the level of galectin correlates with the turnover of biomarkers of extracellular matrix among patients with HFrEF.…”

Section: Discussionmentioning

confidence: 82%

The differences in the relationship between diastolic dysfunction, selected biomarkers and collagen turn-over in heart failure patients with preserved and reduced ejection fraction

et al. 2017

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Background: The aim of the study was to assess the correlation of the selected biomarkers and collagen turn-over indices with advanced echocardiographic parameters among patients with preserved and reduced ejection fraction (EF .6). Clinical evaluation included 6-min walk test, biochemistry, procollagen type I N-terminal propeptide (PINP), procollagen type III N-terminal propetide (PIIINP), matrix metaloproteinase-2 (MMP2), ghrelin, and galectin-3 levels measurements. Echocardiographic examination was performed with analysis of diastolic function and global longitudinal strain (GLS). Results: The GLS in the HFrEF group was significantly lower than in the HFpEF group at the baseline (GLS: 9.56 vs. 16.03, p < 0.01). There was a strong negative correlation of the p = 0.005), but only a moderate negative correlation in p = 0.02). In the HFrEF group, there was a moderate negative correlation between the baseline level of p = 0.03). The correlation of ghrelin and tissue inhibitor of matrix metalloproteinase-1 with EF in the HFrEF group was moderate and statistically significant (r = 0.62, p = 0.02 and r = -0.63, p = 0.02, respectively). Conclusions: Procollagen type III peptide has a strong negative correlation with left ventricular GLS. Galectin-3 relationship with strain may indicate novel pathophysiological pathways and requires further investigation. (Cardiol J 2017; 24, 1: 35-42)

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The relationship between serum galectin-3 and serum markers of cardiac extracellular matrix turnover in heart failure patients

Cited by 139 publications

References 26 publications

Galectin-3 in diabetic patients

Galectin-3 in diabetic patients

Galectin-3 and the Development of Heart Failure after Acute Coronary Syndrome: Pilot Experience from PROVE IT-TIMI 22

The differences in the relationship between diastolic dysfunction, selected biomarkers and collagen turn-over in heart failure patients with preserved and reduced ejection fraction

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