Utility of galectin-3 in predicting post-infarct remodeling after acute myocardial infarction based on extracellular volume fraction mapping

Perea, Rosario J.; Morales-Ruíz, Manuel; Ortiz-Pérez, Josè T.; Bosch, Xavier; Andreu, David; Borràs, Roger; Acosta, Juan; Penela, Diego; Prat-González, Susana; Caralt, Teresa M. de; Martinez, M.; Morales‐Romero, Blai; Lasalvia, Luis; Donnelly, James F.; Jiménez, Wladimiro; Mira, Áurea; Mont, Lluı́s; Berruezo, Antonio

doi:10.1016/j.ijcard.2016.08.070

Cited by 19 publications

(11 citation statements)

References 36 publications

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“…Interestingly, global loss of Gal-3 accelerated cardiac hypertrophy, although the significance of Gal-3 expression in regulation of the biological properties of cardiomyocytes remains unclear 19 . Improvement of cardiac remodeling and decreased LV fibrosis are likely to be linked to the improvement of LV compliance and diastolic function 20–22 . Moreover, heart perfusion occurs during the diastolic phase of the cardiac cycle and therefore can take advantage of improved cardiac compliance.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Ibarrola

Matilla

Martínez‐Martínez

et al. 2019

Sci Rep

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Although optimal therapy for myocardial infarction includes reperfusion to restore blood flow to the ischemic region, ischemia/reperfusion (IR) also initiates an inflammatory response likely contributing to adverse left ventricular (LV) extracellular matrix (ECM) remodeling. Galectin-3 (Gal-3), a β-galactoside-binding-lectin, promotes cardiac remodeling and dysfunction. Our aim is to investigate whether Gal-3 pharmacological inhibition using modified citrus pectin (MCP) improves cardiac remodeling and functional changes associated with IR. Wistar rats were treated with MCP from 1 day before until 8 days after IR (coronary artery ligation) injury. Invasive hemodynamics revealed that both LV contractility and LV compliance were impaired in IR rats. LV compliance was improved by MCP treatment 8 days after IR. Cardiac magnetic resonance imaging showed decreased LV perfusion in IR rats, which was improved with MCP. There was no difference in LV hypertrophy in MCP-treated compared to untreated IR rats. However, MCP treatment decreased the ischemic area as well as Gal-3 expression. Gal-3 blockade paralleled lower myocardial inflammation and reduced fibrosis. These novel data showing the benefits of MCP in compliance and ECM remodeling in IR reinforces previously published data showing the therapeutic potential of Gal-3 inhibition.

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Section: Discussionmentioning

confidence: 99%

Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Ibarrola

Matilla

Martínez‐Martínez

et al. 2019

Sci Rep

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“…Galectin-3 levels were also associated with reinfarction following initial MI ( 72 ). Galectin-3 measured acutely following STEMI was demonstrated as an independent predictor of increased extracellular volume during a 6-month follow-up, which may be useful for long-term risk stratification ( 73 ), and may be used to predict LVEF and infarction size after 4 months when measured immediately following a MI ( 74 ). In addition, serum galectin-3 levels varied significantly following a STEMI over a short time period and were associated with the timing of reperfusion ( 75 ).…”

Section: Galectin-3 and Cardiovascular Diseasementioning

confidence: 99%

Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review)

et al. 2017

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Galectin-3 is a member of the galectin family, which are β-galactoside-binding lectins with ≥1 evolutionary conserved carbohydrate-recognition domain. It binds proteins in a carbohydrate-dependent and -independent manner. Galectin-3 is predominantly located in the cytoplasm; however, it shuttles into the nucleus and is secreted onto the cell surface and into biological fluids including serum and urine. It serves important functions in numerous biological activities including cell growth, apoptosis, pre-mRNA splicing, differentiation, transformation, angiogenesis, inflammation, fibrosis and host defense. Numerous previous studies have indicated that galectin-3 may be used as a diagnostic or prognostic biomarker for certain types of heart disease, kidney disease and cancer. With emerging evidence to support the function and application of galectin-3, the current review aims to summarize the latest literature regarding the biomarker characteristics and potential therapeutic application of galectin-3 in associated diseases.

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“…However, these results are limited by the small size of the study sample (29 STEMI patients). In another small cohort consisting of 26 STEMI patients, Perea et al concluded Gal-3, measured early after MI, is an independent predictor of LV remodeling at 6-month follow-up [48]. In particular, they assessed LV remodeling with extracellular volume fraction (ECV), determined by cardiovascular magnetic resonance (CMR).…”

Section: Gal-3 and Prognosismentioning

confidence: 99%

“…Gal-3 measured acutely after STEMI is an independent predictor of LVR at 6 month followup [48] Di tano et al…”

Section: Prospective 26 Stemi Patientsmentioning

confidence: 99%

Galectin-3 in acute coronary syndrome

Agnello

Bivona

Sasso

et al. 2017

Clinical Biochemistry

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Utility of galectin-3 in predicting post-infarct remodeling after acute myocardial infarction based on extracellular volume fraction mapping

Cited by 19 publications

References 36 publications

Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Myocardial Injury After Ischemia/Reperfusion Is Attenuated By Pharmacological Galectin-3 Inhibition

Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review)

Galectin-3 in acute coronary syndrome

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