Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy

Vergaro, Giuseppe; Franco, Annamaria Del; Giannoni, Alberto; Prontera, Concetta; Ripoli, Andrea; Barison, Andrea; Masci, Pier Giorgio; Aquaro, Giovanni Donato; Solal, Alain Cohen; Padeletti, Luigi; Passino, Claudio; Emdin, Michele

doi:10.1016/j.ijcard.2015.02.008

Cited by 66 publications

(57 citation statements)

References 29 publications

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“…150 patients were collected in a study investigating the relationship between circulating galectin-3 levels and myocardial fibrosis in patients with nonischemic dilated cardiomyopathy (NICM). Galectin-3 value was higher in patients with left ventricular (LV) fibrosis, which supports the view that galectin-3 is related to cardiac fibrosis and remodeling in NICM [25]. In 63 patients with stable coronary artery disease (CAD), gal-3 serum level was determined.…”

Section: Galectin-3mentioning

confidence: 54%

Biomarkers in patients with myocardial fibrosis

Yang

Zheng

et al. 2017

Open Life Sciences

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Section: Galectin-3mentioning

confidence: 54%

Biomarkers in patients with myocardial fibrosis

Yang

Zheng

et al. 2017

Open Life Sciences

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“…More importantly, the occurrence and extent of LGE have been associated with a worse clinical outcome, in particular with impaired ventricular filling and systolic function [83][84][85] and with life-threatening arrhythmias [86][87][88]. A recent study found that galectin-3 predicted the presence and extent of replacement fibrosis at cardiac CMR in a cohort of patients with DCM [89], consistently with the causal role of galectin-3 in the determination of myocardial fibrosis and remodelling. In particular, galectin-3 plasma levels higher than 14.6 ng/mL have been found to predict best the presence of LGE: this value resulted similar to the proposed prognostic cut-off level in a previous study performed on patients with systolic heart failure [47], while other studies provided higher cut-off values [49,90].…”

Section: Late Gadolinium Enhancementmentioning

confidence: 90%

Myocardial interstitial remodelling in non-ischaemic dilated cardiomyopathy: insights from cardiovascular magnetic resonance

et al. 2015

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Myocardial remodelling involves not only the myocytes, but also non-myocyte cells and the extracellular matrix, which constitutes around 6 % of the normal heart and includes fluid, collagen and glycoproteins. In non-ischaemic dilated cardiomyopathy (DCM), the cardiac interstitium increases as a result of diffuse interstitial (microscopic) fibrosis, post-necrotic replacement (macroscopic) fibrosis or myocardial oedema. The activation of the renin-angiotensin-aldosterone system is a major determinant of fibroblasts activation and collagen deposition, with the transforming growth factor β as the downstream signal mediator. Endomyocardial biopsy still represents the current reference method for interstitial and replacement myocardial fibrosis assessment, but cardiovascular magnetic resonance (CMR) allows in vivo detection of macroscopic fibrosis with post-contrast late enhancement imaging. Moreover, recent pre- and post-contrast T1 mapping techniques provide a quantitative estimation of myocardial interstitial remodelling, with potential diagnostic and prognostic clinical utility. Here, we review the pathophysiological mechanisms of myocardial interstitial remodelling in DCM, its non-invasive characterization with biomarkers and with CMR, as well as the most recent studies about their clinical utility.

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“…Characterized by enlarged ventricular dimensions and systolic dysfunction (2), DCM is the most frequent type of cardiomyopathy, accounting for 10% of the newly diagnosed heart failure cases (3). Management of DCM is an economic burden worldwide (4). Therefore, it is urgent to identify the genetic etiologies of this disease.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell-derived cardiomyocyte model

Gong

Zhong

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Dilated cardiomyopathy (DCM) is the most common type of cardiomyopathy that account for the majority of heart failure cases. The present study aimed to reveal the underlying molecular mechanisms of DCM and provide potential biomarkers for detection of this condition. The public dataset of GSE35108 was downloaded, and 4 normal induced pluripotent stem cell (iPSC)-derived cardiomyocytes (N samples) and 4 DCM iPSC-derived cardiomyocytes (DCM samples) were utilized. Raw data were preprocessed, followed by identification of differentially expressed genes (DEGs) between N and DCM samples. Crucial functions and pathway enrichment analysis of DEGs were investigated, and protein-protein interaction (PPI) network analysis was conducted. Furthermore, a module network was extracted from the PPI network, followed by enrichment analysis. A set of 363 DEGs were identified, including 253 upregulated and 110 downregulated genes. Several biological processes (BPs), such as blood vessel development and vasculature development (FLT1 and MMP2), cell adhesion (CDH1, ITGB6, COL6A3, COL6A1 and LAMC2) and extracellular matrix (ECM)-receptor interaction pathway (CDH1, ITGB6, COL6A3, COL6A1 and LAMC2), were significantly enriched by these DEGs. Among them, MMP2, CDH1 and FLT1 were hub nodes in the PPI network, while COL6A3, COL6A1, LAMC2 and ITGB6 were highlighted in module 3 network. In addition, PENK and APLNR were two crucial nodes in module 2, which were linked to each other. In conclusion, several potential biomarkers for DCM were identified, such as MMP2, FLT1, CDH1, ITGB6, COL6A3, COL6A1, LAMC2, PENK and APLNR. These genes may serve significant roles in DCM via involvement of various BPs, such as blood vessel and vasculature development and cell adhesion, and the ECM-receptor interaction pathway.

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Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy

Cited by 66 publications

References 29 publications

Biomarkers in patients with myocardial fibrosis

Biomarkers in patients with myocardial fibrosis

Myocardial interstitial remodelling in non-ischaemic dilated cardiomyopathy: insights from cardiovascular magnetic resonance

Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell-derived cardiomyocyte model

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