Galectin-3 and post-myocardial infarction cardiac remodeling

Meijers, Wouter C.; Velde, A. Rogier van der; Pascual-Figal, Domingo A.; Boer, Rudolf A. de

doi:10.1016/j.ejphar.2015.06.025

Cited by 68 publications

(73 citation statements)

References 65 publications

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“…This assumption is supported by laboratory data [17]. Accordingly, one might expect a relationship between Gal-3, infarct size, infarct healing and LV remodeling in patients with MI, although previous clinical studies on this topic are equivocal [17]. The aim of this study was to study circulating levels of Gal-3 in patients with acute ST-elevation MI (STEMI) and patients with previous complicated MI, and to explore the relationship between Gal-3, MI size and the parameters of LV remodeling assessed by cardiac magnetic resonance (CMR) imaging.…”

Section: Introductionsupporting

confidence: 65%

“…Both these processes, which are pivotal after acute MI, might theoretically cause an upregulation of Gal-3. This assumption is supported by laboratory data [17]. Accordingly, one might expect a relationship between Gal-3, infarct size, infarct healing and LV remodeling in patients with MI, although previous clinical studies on this topic are equivocal [17].…”

Section: Introductionsupporting

confidence: 63%

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Circulating Galectin-3 Levels Are Increased in Patients with Ischemic Heart Disease, but Are Not Influenced by Acute Myocardial Infarction

Singsaas

Manhenke²,

Dickstein³

et al. 2016

Cardiology

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Objectives: Galectin-3 (Gal-3) is involved in cardiac inflammation and fibrosis, and is in use as a biomarker that indicates increased risk in heart failure. This study examined the relationship between Gal-3 levels and acute and old myocardial infarction (MI) in patients assessed by cardiac magnetic resonance (CMR) imaging. Methods: Group 1 consisted of 38 patients with ST-elevation MI and single-vessel disease treated with primary percutaneous coronary intervention (PCI). Group 2 consisted of 52 patients with prior complicated MI. Twenty-two controls were included. CMR was performed in group 1 at 2 days, 1 week, 2 months and 1 year following PCI and in group 2 at >4 years after MI. Results: Median Gal-3 was elevated in patients compared with controls, group 1: 11.93 ng/ml (IQR 6.34-17.52, p = 0.03), group 2: 12.96 (IQR 6.33-19.29, p = 0.03) and controls: 10.16 (IQR 5.59-14.73). Gal-3 levels did not change during acute MI, and there was no relationship between Gal-3 and infarct size, troponin-T, high-sensitivity C-reactive protein, left-ventricular (LV) volumes or LV ejection fraction (LVEF) in group 1. In group 2, Gal-3 correlated modestly with MI size (r = 0.28, p < 0.05), LV end-diastolic volume index (r = 0.40, p < 0.01), LV end-systolic volume index (r = 0.43, p < 0.01) and LVEF (r = -0.39, p < 0.01). Conclusion: There was no relationship between Gal-3 levels and acute ischemic myocardial injury. A significant, modest relationship between Gal-3 levels, MI size and LV remodeling was only found in patients with old MI.

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Section: Introductionsupporting

confidence: 65%

Section: Introductionsupporting

confidence: 63%

Circulating Galectin-3 Levels Are Increased in Patients with Ischemic Heart Disease, but Are Not Influenced by Acute Myocardial Infarction

Singsaas

Manhenke²,

Dickstein³

et al. 2016

Cardiology

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“…Cardiac remodeling occurs after myocardial infarction, which is manifested as the disordered arrangement of myocardial cells and significant increase of myocardial fibrosis in heart morphology (19). In this study, myocardial cells were arranged disorderly and myocardial fibrosis was obvious with cardiac remodeling in non-infarcted zone in Sal group.…”

Section: Discussionmentioning

confidence: 99%

Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats

et al. 2018

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The effects of berberine on cardiac function of heart failure after myocardial infarction and its possible mechanism were investigated. The anterior descending branches of 50 female Wistar rats were ligatured to establish the model of heart failure after myocardial infarction. At 4 weeks after successful modeling, the rats were randomly divided into two groups receiving 4-week gavage with saline (Sal group) and berberine (Ber group), while the sham-operation group (Sham group) was set up. After 4 weeks, the hemodynamics and serum BNP in rats were measured. The hearts of rats were taken to detect the degree of myocardial fibrosis. The myocardial cell apoptosis was detected. The expressions and changes in myocardial apoptosis-related proteins, including Bcl-2, Bax and caspase-3, were detected. The expression and changes in GRP78, CHOP and caspase-12 in myocardial tissue were detected. The results showed that Berberine improved the cardiac function of rats after myocardial infarction. After myocardial infarction, myocardial fibrosis and apoptosis were observed around the infarction area, berberine improved the myocardial fibrosis and reduced cell apoptosis. Furthermore, berberine alleviated endoplasmic reticulum stress (ERS) after myocardial infarction. In conclusion, Berberine can inhibit the myocardium cell apoptosis of heart failure after myocardial infarction, and its mechanism may be realized by affecting the ERS in myocardial tissue of heart failure after myocardial infarction and CHOP and caspase-12 apoptotic signaling pathway, upregulating Bcl-2/Bax expression and downregulating caspase-3 expression, thus inhibiting the cardiac remodeling and protecting the cardiac function.

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“…MI causes complex alterations in the architecture and function of the left ventricle (LV), named "LV remodeling" (LVR), involving both the infarcted and non-infarcted myocardium [44]. LVR occurs initially as a compensatory mechanism but later it can lead to adverse LVR resulting in LV dysfunction and HF.…”

Section: Gal-3 and Prognosismentioning

confidence: 99%