NOD1 receptor is up-regulated in diabetic human and murine myocardium

Prieto, Patricia; Vallejo‐Cremades, María Teresa; Benito, Gemma; González‐Peramato, Pilar; Francés, Daniel E.; Agra, Noelia; Terrón, Verónica; González-Ramos, Silvia; Delgado, Carmen; Ruiz‐Gayo, Mariano; Pacheco, Ivette; Velasco-Martín, Juan P.; Regadera, Javier; Martı́n-Sanz, Paloma; López-Collazo, Eduardo; Fernández‐Velasco, María

doi:10.1042/cs20140180

Cited by 20 publications

(15 citation statements)

References 56 publications

(54 reference statements)

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“…So far, only a limited number of studies in vivo have shown the effect of NOD1 in the cardiovascular field (23)(24)(25)(26). Consistent with a previous report (27), we here establish that Nod1 deficiency prevents early atherosclerosis development in Apoe 2/2 mice.…”

Section: Discussionsupporting

confidence: 92%

Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1

et al. 2018

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Atherosclerosis is a chronic disease characterized by vascular lipid retention and inflammation, and pattern recognition receptors (PRRs) are important contributors in early stages of the disease. Given the implication of the intracellular PRR nucleotide‐binding oligomerization domain 1 (NOD1) in cardiovascular diseases, we investigated its contribution to early atherosclerosis. We evidenced NOD1 induction in atherosclerotic human and mouse tissues, predominantly in vascular endothelial cells. Accordingly, NOD1 genetic inactivation in Apoe−/− mice reduced not only atherosclerosis burden, but also monocyte and neutrophil accumulation in atheromata. Of note, in the presence of either peptidoglycan or oxidized LDLs, endothelial NOD1 triggered VCAM‐1 up‐regulation through the RIP2‐NF‐κB axis in an autocrine manner, enhancing firm adhesion of both sets of myeloid cells to the inflamed micro‐ and macro vasculature in vivo. Our data define a major proatherogenic role for endothelial NOD1 in early leukocyte recruitment to the athero‐prone vasculature, thus introducing NOD1 as an innovative therapeutic target and potential prognostic molecule.—González‐Ramos, S., Paz‐García, M., Rius, C., del Monte‐Monge, A., Rodríguez, C., Fernández‐García, V., Andrés, V., Martínez‐González, J., Lasunción, M. A., Martín‐Sanz, P., Soehnlein, O., Boscá, L. Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1. FASEB J. 33, 3912–3921 (2019). http://www.fasebj.org

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Section: Discussionsupporting

confidence: 92%

Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1

et al. 2018

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“…164 In addition, NOD1 expression is upregulated in heart tissues and cardiomyocytes of mice with T2DM, implying a possible role of NOD1 in diabetic cardiomyopathy. 165 ALRs are one of the newly characterized superfamilies of PRRs that recognize endogenous and exogenous DNA, such as poly (dA-dT) and vaccinia virus double stranded DNA. [167][168][169] Functionally, ALRs regulate inflammasome assembly, and cell differentiation, proliferation, and apoptosis.…”

Section: Nlrs In Diabetic Cardiomyopathymentioning

confidence: 99%

Pattern recognition receptor‐mediated inflammation in diabetic vascular complications

Wang

Antony

Wang

et al. 2020

Medicinal Research Reviews

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The innate immune system contains multiple classes of pattern recognition receptors (PRRs), which recognize pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the intracellular and extracellular space. Although PRRs are indispensable for the detection and clearance of invading pathogens, dysregulated PRR activation by extrinsic and intrinsic factors leads to inflammatory diseases. PRRmediated inflammation has been shown to play a pivotal role in the pathogenesis of diabetic vascular complications (DVCs), which are the leading causes of morbidity and mortality in diabetic patients. Upon sensing hyperglycemiagenerated DAMPs, PRRs activate intracellular signaling pathways leading to the production of proinflammatory cytokines and chemokines in various cells of the kidney, brain, eye, and heart. The resulting chronic, low-grade inflammation contributes to DVCs. In this review, we summarize the role of PRRs in DVCs including diabetic nephropathy, neuropathy, retinopathy, and cardiomyopathy. We propose that targeting PRRs and associated signaling pathways may be beneficial for the management of DVCs.

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“…Nucleotide oligomerization-binding domain 1 (NOD1) is an innate immune receptor that is involved in the pathogenesis of diabetes in various organs, including the heart. Although increased NOD-1 is associated increased levels of NF-κB and apoptosis in diabetic mice, its underlying contribution still remains poorly understood [71]. NOD1 is found in cardiac fibroblasts, with levels increased in cardiac fibroblasts from Lepr db/db mice compared to non-diabetic controls [72].…”

Section: Nucleotide Oligomerization-binding Domainmentioning

confidence: 99%

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

Levick

Widiapradja

2020

IJMS

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Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately result in heart failure with preserved ejection fraction. Cardiac fibroblasts are the final effector cell in the process of cardiac fibrosis. This review article aims to describe the cardiac fibroblast phenotype in response to high-glucose conditions that mimic the diabetic state, as well as to explain the pathways underlying this phenotype. As such, this review focuses on studies conducted on isolated cardiac fibroblasts. We also describe molecules that appear to oppose the pro-fibrotic actions of high glucose on cardiac fibroblasts. This represents a major gap in knowledge in the field that needs to be addressed.

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NOD1 receptor is up-regulated in diabetic human and murine myocardium

Abstract: We demonstrate that the myocardium from murine models of diabetes and the myocardium of patients with Type 2 diabetes overexpress the receptor of the innate immune system NOD1. This up-regulation occurred in cardiomyocytes and was associated with an increased apoptotic profile.

Cited by 20 publications

References 56 publications

Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1

Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1

Pattern recognition receptor‐mediated inflammation in diabetic vascular complications

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

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