Mannose-Binding Lectin Levels and Carotid Intima-Media Thickness in Type 2 Diabetic Patients

Káplár, Miklós; Shah, Sweni; Kulcsar, J.; Cogoi, B.; Esze, Regina; Somodi, Sándor; Papp, Mária; Oláh, László; Magyar, Mária Tünde; Szabó, Katalin; Czuriga-Kovács, Katalin Réka; Hársfalvi, Jolán; Paragh, György

doi:10.1155/2016/8132925

Cited by 12 publications

(12 citation statements)

References 43 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, although alternative interpretations cannot be excluded, i.e., that MBL is not consumed due to a lack of involvement in the condition, the overall data may indicate the association of MBL with plaque instability. This observation extends the concept that MBL in atherosclerosis may have different effects depending on time in the disease process and the specific clinical setting ( 29 , 32 ).…”

Section: Discussionsupporting

confidence: 80%

“…Of the pathways of complement system activation, the classical and alternative have a dual function in atherosclerosis, counteracting plaque formation through debris clearance or favoring atherogenesis ( 12 ). Less is known on the role of the LP that may have either an anti-atherogenic ( 24 – 27 ) or a pro-atherogenic ( 29 – 31 ) and pro-thrombotic function ( 12 ).…”

Section: Discussionmentioning

confidence: 99%

“…In line with these data, Vengen et al showed that the presence of MBL variant allele may increase the risk of myocardial infarction in young individuals ( 32 ) and Saevarsdottir proposed for MBL an anti-atherogenic role ( 28 ). On the other hand, high MBL serum levels are associated with increased risk of coronary artery disease in men ( 30 ) and in diabetic patients ( 29 ). Moreover, patients with normal MBL genotype are more likely to experience restenosis after endarterectomy ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

“…The LP is activated by the initiator molecules mannose-binding lectin (MBL), ficolins (ficolin-1 or M-ficolin, ficolin-2 or L-ficolin, and ficolin-3 or H-ficolin), and collectin-11 ( 21 – 23 ). A few studies reported MBL involvement in atherosclerosis, though results are contrasting, supporting either an anti-atherogenic ( 24 – 28 ) or a pro-atherogenic ( 29 – 31 ) role. A few data are available on the LP involvement in plaque vulnerability ( 32 ), with still open questions.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Lectin Pathway of Complement Activation Is Associated with Vulnerability of Atherosclerotic Plaques

et al. 2017

View full text Add to dashboard Cite

Inflammatory mechanisms may be involved in atherosclerotic plaque rupture. By using a novel histology-based method to quantify plaque instability here, we assess whether lectin pathway (LP) of complement activation, a major inflammation arm, could represent an index of plaque instability. Plaques from 42 consecutive patients undergoing carotid endarterectomy were stained with hematoxylin-eosin and the lipid core, cholesterol clefts, hemorrhagic content, thickness of tunica media, and intima, including or not infiltration of cellular debris and cholesterol, were determined. The presence of ficolin-1, -2, and -3 and mannose-binding lectin (MBL), LP initiators, was assessed in the plaques by immunofluorescence and in plasma by ELISA. LP activation was assessed in plasma by functional in vitro assays. Patients presenting low stenosis (≤75%) had higher hemorrhagic content than those with high stenosis (>75%), indicating increased erosion. Increased hemorrhagic content and tunica media thickness, as well as decreased lipid core and infiltrated content were associated with vulnerable plaques and therefore used to establish a plaque vulnerability score that allowed to classify patients according to plaque vulnerability. Ficolins and MBL were found both in plaques’ necrotic core and tunica media. Patients with vulnerable plaques showed decreased plasma levels and intraplaque deposition of ficolin-2. Symptomatic patients experiencing a transient ischemic attack had lower plasma levels of ficolin-1. We show that the LP initiators are present within the plaques and their circulating levels change in atherosclerotic patients. In particular, we show that decreased ficolin-2 levels are associated with rupture-prone vulnerable plaques, indicating its potential use as marker for cardiovascular risk assessment in atherosclerotic patients.

show abstract

Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Lectin Pathway of Complement Activation Is Associated with Vulnerability of Atherosclerotic Plaques

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Other important differences were evident. Pemafibrate (but not fenofibric acid) upregulated the genes encoding mannose-binding lectin 2 ( MBL2), involved in regulation of the innate immune system, inflammation and, possibly, vascular complications in diabetes [ 46 , 47 ], as well as glutamyl aminopeptidase ( ENPEP ), involved in regulation of blood pressure [ 48 ], in transcriptome analysis [ 43 ]. In addition, pemafibrate induced expression of fibroblast growth factor 21 ( FGF21) to a greater extent than fenofibric acid [ 43 ].…”

Section: A Novel Spparmα: Pemafibrate (K-877)mentioning

confidence: 99%

Pemafibrate (K-877), a novel selective peroxisome proliferator-activated receptor alpha modulator for management of atherogenic dyslipidaemia

Fruchart¹

2017

Cardiovasc Diabetol

120

View full text Add to dashboard Cite

Despite best evidence-based treatment including statins, residual cardiovascular risk poses a major challenge for clinicians in the twenty first century. Atherogenic dyslipidaemia, in particular elevated triglycerides, a marker for increased triglyceride-rich lipoproteins and their remnants, is an important contributor to lipid-related residual risk, especially in insulin resistant conditions such as type 2 diabetes mellitus. Current therapeutic options include peroxisome proliferator-activated receptor alpha (PPARα) agonists, (fibrates), but these have low potency and limited selectivity for PPARα. Modulating the unique receptor–cofactor binding profile to identify the most potent molecules that induce PPARα-mediated beneficial effects, while at the same time avoiding unwanted side effects, offers a new therapeutic approach and provides the rationale for development of pemafibrate (K-877, Parmodia™), a novel selective PPARα modulator (SPPARMα). In clinical trials, pemafibrate either as monotherapy or as add-on to statin therapy was effective in managing atherogenic dyslipidaemia, with marked reduction of triglycerides, remnant cholesterol and apolipoprotein CIII. Pemafibrate also increased serum fibroblast growth factor 21, implicated in metabolic homeostasis. There were no clinically meaningful adverse effects on hepatic or renal function, including no relevant serum creatinine elevation. A major outcomes study, PROMINENT, will provide definitive evaluation of the role of pemafibrate for management of residual cardiovascular risk in type 2 diabetes patients with atherogenic dyslipidaemia despite statin therapy.

show abstract

Influence of the treatment of periodontal disease in serum concentration of sirtuin 1 and mannose‐binding lectin

Caribé

Villar

Romito

et al. 2020

Journal of Periodontology

View full text Add to dashboard Cite

BackgroundIncreased levels of periodontal pathogens disrupt the homeostasis between the host and its microbiota and increase susceptibility to periodontal diseases. Periodontitis increases the serum concentration of mannose‐binding lectin (MBL), which exacerbates local inflammatory processes. In animal studies, sirtuin 1 (SIRT1) was associated with protection against inflammation. This study analyzed the influence of non‐surgical periodontal treatment on serum levels of MBL and SIRT1.MethodsForty patients with periodontitis and 38 periodontally healthy individuals (aged 45 to 79 years) were included. Periodontitis patients received scaling and root planing using machine driven and hand instruments. Clinical parameters, inflammatory biomarkers, MBL, and SIRT1 levels were measured at baseline and at post‐treatment.ResultsFor all patients, an inverse correlation was observed between serum concentrations of MBL and SIRT1 (r = ‐0.30; P = 0.006). Periodontal treatment reduced serum concentrations of MBL (1,099.35 ± 916.59 to 861.42 ± 724.82 ng/mL; P < 0.001) and C‐reactive protein (6.05 ± 8.99 to 2.49 ± 2.89 mg/L; P = 0.009). By contrast, SIRT1 serum levels increased (1.06 ± 1.03 to 1.66 ± 1.64 ng/mL; P < 0.001) following periodontal treatment.ConclusionsPeriodontal treatment was associated with decreased serum concentrations of MBL and CRP and increased serum levels of SIRT1. Prospective studies are needed to assess the impact of these biomarkers on pathophysiology of periodontitis.

show abstract

Mannose-Binding Lectin Levels and Carotid Intima-Media Thickness in Type 2 Diabetic Patients

Cited by 12 publications

References 43 publications

Lectin Pathway of Complement Activation Is Associated with Vulnerability of Atherosclerotic Plaques

Lectin Pathway of Complement Activation Is Associated with Vulnerability of Atherosclerotic Plaques

Pemafibrate (K-877), a novel selective peroxisome proliferator-activated receptor alpha modulator for management of atherogenic dyslipidaemia

Influence of the treatment of periodontal disease in serum concentration of sirtuin 1 and mannose‐binding lectin

Contact Info

Product

Resources

About