Differences in galectin-3, a biomarker of fibrosis, between participants with peripheral artery disease and participants with normal ankle–brachial index

Casanegra, Ana I.; Stoner, Julie A.; Tafur, Alfonso; Pereira, Héléna; Rathbun, Suman; Gardner, Andrew W.

doi:10.1177/1358863x16644059

Cited by 11 publications

(13 citation statements)

References 39 publications

(59 reference statements)

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“…Our findings are consistent with several proposed mechanisms of PAD progression, and confirm their importance in a relevant human study [ 29 , 30 , 31 ]. For example, TGFβ produced by vascular smooth muscle cells predicts fibrosis in the gastrocnemius of patients with PAD [ 30 ].…”

Section: Discussionsupporting

confidence: 92%

Fibrosis Distinguishes Critical Limb Ischemia Patients from Claudicants in a Transcriptomic and Histologic Analysis

Cong

Cui

Ferrari

et al. 2020

JCM

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Most patients with critical limb ischemia (CLI) from peripheral arterial disease (PAD) do not have antecedent intermittent claudication (IC). We hypothesized that transcriptomic analysis would identify CLI-specific pathways, particularly in regards to fibrosis. Derivation cohort data from muscle biopsies in PAD and non-PAD (controls) was obtained from the Gene Expression Omnibus (GSE120642). Transcriptomic analysis indicated CLI patients (N = 16) had a unique gene expression profile, when compared with non-PAD controls (N = 15) and IC (N = 20). Ninety-eight genes differed between controls and IC, 2489 genes differed between CLI and controls, and 2783 genes differed between CLI and IC patients. Pathway enrichment analysis showed that pathways associated with TGFβ, collagen deposition, and VEGF signaling were enriched in CLI but not IC. Receiver operating curve (ROC) analysis of nine fibrosis core gene expression revealed the areas under the ROC (AUC) were all >0.75 for CLI. Furthermore, the fibrosis area (AUC = 0.81) and % fibrosis (AUC = 0.87) in validation cohort validated the fibrosis discrimination CLI from IC and control (all n = 12). In conclusion, transcriptomic analysis identified fibrosis pathways, including those involving TGFβ, as a novel gene expression feature for CLI but not IC. Fibrosis is an important characteristic of CLI, which we confirmed histologically, and may be a target for novel therapies in PAD.

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Section: Discussionsupporting

confidence: 92%

Fibrosis Distinguishes Critical Limb Ischemia Patients from Claudicants in a Transcriptomic and Histologic Analysis

Cong

Cui

Ferrari

et al. 2020

JCM

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“…Alterations in plasma galectin-3 concentrations in PAD have been investigated by two independent research groups. Casanegra et al [ 35 ] analyzed galectin-3 in 29 patients attending the Mayo Clinics with no evidence of PAD (normal ankle brachial index; ABI), and 31 patients with PAD (low ABI). They observed a mean galectin-3 concentration of 14.4 ng/mL in subjects with normal ABI, and approximately 22% increase in PAD patients.…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 in Peripheral Artery Disease. Relationships with Markers of Oxidative Stress and Inflammation

Fort-Gallifa

Hernández-Aguilera

García-Heredia

et al. 2017

IJMS

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Galectin-3 is a modulator of oxidative stress, inflammation, and fibrogenesis involved in the pathogenesis of vascular diseases. The present study sought to characterize, in patients with peripheral artery disease (PAD), the localization of galectin-3 in arterial tissue, and to analyze the relationships between the circulating levels of galectin-3 and oxidative stress and inflammation. It also sought to compare the diagnostic accuracy of galectin-3 with that of other biochemical markers of this disease. We analyzed femoral or popliteal arteries from 50 PAD patients, and four control arteries. Plasma from 86 patients was compared with that from 72 control subjects. We observed differences in the expression of galectin-3 in normal arteries, and arteries from patients with PAD, with a displacement of the expression from the adventitia to the media, and the intima. In addition, plasma galectin-3 concentration was increased in PAD patients, and correlated with serologic markers of oxidative stress (F2-isoprostanes), and inflammation [chemokine (C−C motif) ligand 2, C-reactive protein, β-2-microglobulin]. We conclude that the determination of galectin-3 has good diagnostic accuracy in the assessment of PAD and compares well with other analytical parameters currently in use.

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“…Patients exhibiting peripheral artery disease also demonstrated increased galectin-3 levels, and galectin-3 was positively associated with homeostatic model assessment, but not arterial elasticity and microalbuminuria following adjustment for age and sex ( 95 ). A prospective observational study indicated that elevated plasma galectin-3 levels were markedly associated with inflammation, severity and poor prognosis following intracerebral hemorrhage ( 96 ).…”

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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Differences in galectin-3, a biomarker of fibrosis, between participants with peripheral artery disease and participants with normal ankle–brachial index

Cited by 11 publications

References 39 publications

Fibrosis Distinguishes Critical Limb Ischemia Patients from Claudicants in a Transcriptomic and Histologic Analysis

Fibrosis Distinguishes Critical Limb Ischemia Patients from Claudicants in a Transcriptomic and Histologic Analysis

Galectin-3 in Peripheral Artery Disease. Relationships with Markers of Oxidative Stress and Inflammation

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

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