Galectin-3 mediates the pulmonary arterial hypertension–induced right ventricular remodeling through interacting with NADPH oxidase 4

He, Jingsong; Li, Xiaohui; Luo, Hui; Li, Tangzhiming; Zhao, Lin; Qi, Qiangqiang; Liu, Yu-wei; Yu, Zaixin

doi:10.1016/j.jash.2017.03.008

Cited by 62 publications

(52 citation statements)

References 40 publications

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“…Moreover, galectin‐3 increased peroxide, nitrotyrosine, malondialdehyde, and N ‐carboxymethyl‐lysine levels and decreased total antioxidant capacity . In addition, galectin‐3 was also reported to increase the expression of Nox4 in cardiac cells and regulate Nox4‐derived ROS levels during cardiac fibrosis . Therefore, reducing oxidative stress and improving antioxidant defences by inhibiting galectin‐3 could be a promising approach to reduce cardiac damage in HF.…”

Section: Regulatory Mechanism Of Galectin‐3 In Cardiac Fibrosismentioning

confidence: 99%

The role of galectin‐3 in heart failure and cardiovascular disease

Zhong

Qian

Chen

et al. 2019

Clin Exp Pharma Physio

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Summary Galectin‐3, a β‐galactoside‐binding lectin, is a new important player in the progression of heart failure (HF) and is also linked to poor outcome in patients with cardiovascular disease. Genetic or pharmacological inhibition of galectin‐3 slows down the progression of myocardial inflammation, reduces collagen production, attenuates cardiac remodelling, and ameliorates cardiac function. In this review, we summarize recent progress in research on galectin‐3 as a regulatory molecule involved in cardiovascular fibrosis in HF and its potential role in the diagnosis, risk assessment and treatment of cardiovascular diseases.

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Section: Regulatory Mechanism Of Galectin‐3 In Cardiac Fibrosismentioning

confidence: 99%

The role of galectin‐3 in heart failure and cardiovascular disease

Zhong

Qian

Chen

et al. 2019

Clin Exp Pharma Physio

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“…Additionally, a new line of evidence points out that Gal-3 is involved in reactive oxygen species (ROS) production, although the mechanisms have not been elucidated. Gal-3 increases the expression of Nox4 in cardiac cells and could regulate Nox4-derived ROS levels during cardiac fibrosis [19]. Moreover, Gal-3 downregulates peroxiredoxin-4 inducing a decrease in total antioxidant capacity and a consequent increase in peroxide production and in oxidative stress markers in cardiac fibroblasts [20].…”

Section: Galectin-3 21 Galectin-3 Induces Fibrosis Inflammation Anmentioning

confidence: 99%

“…The axis Aldo/Gal-3 is relevant in pulmonary arterial hypertension because plasma levels of both molecules are associated with pulmonary arterial hypertension severity [40]. Furthermore, Gal-3 positively correlated with Nox4 (related to oxidative stress production) in pulmonary arterial hypertension patients [41].…”

Section: Aldosterone-galectin-3 In Clinical Populationsmentioning

confidence: 99%

Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling

Ibarrola¹,

Jaisser²,

López‐Andrés³

2019

Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine

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The incidence of heart failure (HF) is increasing because of aging of the population. Despite optimal therapy, patients with HF experience disease progression associated with high mortality rates. HF is still the first cause of hospital admission in subjects aged >65 years. The obvious solution for HF epidemics is to prevent new-onset HF with therapies directed specifically to mechanistic targets that are involved in the transition to HF. The mineralocorticoid receptor (MR) and its natural ligand, the hormone aldosterone (Aldo), play important roles during cardiac and arterial remodeling, but the underlying effects are still not understood. MR antagonists are highly recommended for treatment of systolic symptomatic HF. However, adverse effects limit their use in clinical practice. Galectin-3 (Gal-3), neutrophil gelatinase-associated lipocalin (NGAL), and cardiotrophin-1 (CT-1) have been identified as highly focused targets controlling downstream key MR-mediated HF mechanisms. Therefore, interfering with mechanistic pathways involved in downstream MR activation may provide therapeutic alternatives to MR antagonists. The aim of this review is to focus on the role of the MR biotargets in cardiovascular remodeling.

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“…that Gal-3 was up-regulated in adventitia of pulmonary arteries of hypoxia-induced PAH and it regulated the proliferation, differentiation, and accumulation of extracellular matrix by synthesis of collagen and other fibrotic components (Luo, H. et al, 2017). Gal-3 exhibited pro-fibrotic effects interacting of platelet-derived growth factor (Guo, S., & Feng, Z., 2015), transforming growth factor-beta-1 (TGF-β1), matrix metalloproteinase-9 (MMP-9) (Wang, X. et al, 2017) and NADPH oxidase 4 (He, J. et al, 2017a). Interestingly, TGF-β1 was able to promote the expression of Gal-3 and its translocation, while blockage of STAT3 suppressed the expression of Gal-3 induced by TGF-β1 (He, J. et al, 2017a).…”

Section: Introductionmentioning

confidence: 99%

“…Gal-3 exhibited pro-fibrotic effects interacting of platelet-derived growth factor (Guo, S., & Feng, Z., 2015), transforming growth factor-beta-1 (TGF-β1), matrix metalloproteinase-9 (MMP-9) (Wang, X. et al, 2017) and NADPH oxidase 4 (He, J. et al, 2017a). Interestingly, TGF-β1 was able to promote the expression of Gal-3 and its translocation, while blockage of STAT3 suppressed the expression of Gal-3 induced by TGF-β1 (He, J. et al, 2017a). Thus, TGF-β1-dependent vascular fibrosis is mediated by Gal-3 / MMP-9 / STAT3 signaling cascade.…”

Section: Introductionmentioning

confidence: 99%

Emerging Role of Galectin-3 in Pulmonary Artery Hypertension

Berezin¹

2018

MHS

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Pulmonary arterial hypertension (PAH) is multifactorial disadptive disease with poor clinical outcomes associated with increased pulmonary artery pressure resulting in primary small-to-moderate pulmonary artery remodeling. Numerous factors, including smooth muscle cell proliferation, vasospasm, vascular fibrosis and occlusion, direct vascular injury and inflammation, impaired repair of vasculature, are involved in the pathogenesis of PAH. It has been suggested that galectin-3 as a biomarker of excessive fibrosis and inflammation can be useful predictor of both severity and prognosis in patient with PAH. The short communication is reported that elevated Gal-3 levels were found in majority patients with PAH depending on clinical status and of the disease. Although elevated Gal-3 levels were associated with a higher risk of all-cause mortality, cardiovascular mortality, and right ventricle heart failure, the value of this biomarker in PAH patients at high risk stratification is uncertain and requires to be investigated in large clinical trials.

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Galectin-3 mediates the pulmonary arterial hypertension–induced right ventricular remodeling through interacting with NADPH oxidase 4

Cited by 62 publications

References 40 publications

The role of galectin‐3 in heart failure and cardiovascular disease

The role of galectin‐3 in heart failure and cardiovascular disease

Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling

Emerging Role of Galectin-3 in Pulmonary Artery Hypertension

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