Galectin-3 mediates pulmonary vascular remodeling in hypoxia-induced pulmonary arterial hypertension

Luo, Hui; Liu, Bin; Zhao, Lin; He, Jingsong; Li, Tangzhiming; Zha, Lihuang; Li, Xiaohui; Qi, Qiangqiang; Liu, Yuwei; Yu, Zaixin

doi:10.1016/j.jash.2017.07.009

Cited by 39 publications

(38 citation statements)

References 36 publications

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“…Furthermore, Luo et al corroborated that hypoxic condition in PAH triggers gal3 levels, promoting cell proliferation, inflammatory response and fibrotic driven tissue remodeling (61). In the same study, inhibition of gal3 reduced PAH (61). Similarly, Fulton and colleagues demonstrated that genetic or pharmacological inhibition of gal3 resulted in reduced pulmonary hypertension in vivo in a model of hypoxiainduced PAH (62).…”

Section: Galectin-3 As a Biomarker And Therapeutic Target In Covid-19mentioning

confidence: 87%

“…Using small transferring RNA to inhibit gal3, they reduced the increased ventricular pressure, hypoxia-induced inflammatory response and alleviated ventricle hypertrophy of mice with hypoxia-induced PAH (60). Furthermore, Luo et al corroborated that hypoxic condition in PAH triggers gal3 levels, promoting cell proliferation, inflammatory response and fibrotic driven tissue remodeling (61). In the same study, inhibition of gal3 reduced PAH (61).…”

Section: Galectin-3 As a Biomarker And Therapeutic Target In Covid-19mentioning

confidence: 90%

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Hyperinflammation and Fibrosis in Severe COVID-19 Patients: Galectin-3, a Target Molecule to Consider

et al. 2020

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COVID-19 disease have become so far the most important sanitary crisis in the XXI century. In light of the events, any clinical resource should be considered to alleviate this crisis. Severe COVID-19 cases present a so-called cytokine storm as the most life-threatening symptom accompanied by lung fibrosis. Galectin-3 has been widely described as regulator of both processes. Hereby, we present compelling evidences on the potential role of galectin-3 in COVID-19 in the regulation of the inflammatory response, fibrosis and infection progression. Moreover, we provide a strong rationale of the utility of measuring plasma galectin-3 as a prognosis biomarker for COVID-19 patients and propose that inhibition of galectin-3 represents a feasible and promising new therapeutical approach.

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Section: Galectin-3 As a Biomarker And Therapeutic Target In Covid-19mentioning

confidence: 87%

Section: Galectin-3 As a Biomarker And Therapeutic Target In Covid-19mentioning

confidence: 90%

Hyperinflammation and Fibrosis in Severe COVID-19 Patients: Galectin-3, a Target Molecule to Consider

et al. 2020

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“…The aim of the short communication is to summarize knowledge regarding the role of galectin-3 in risk stratification of PAH patients. 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).…”

Section: Introductionmentioning

confidence: 94%

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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“…The authors found that pirfenidone treatment of pulmonary artery-banded mice reduced the amount of fibrosis but did not restore RV function. Because the pro-fibrotic galectin-3 and elevation of circulating galectin-3 have been linked to the development of left heart failure and RV dysfunction (3–5), the authors focused their attention on galectin-3 to explain the (lack of) importance of RV fibrosis in RV failure.…”

mentioning

confidence: 99%