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Article: CCL17 and CCL22 chemokines are upregulated in human obesity and play a role in vascular dysfunction.

Hueso, Luisa / Marques, Patrice / Morant, Brenda / Gonzalez-Navarro, Herminia / Ortega, Joaquin / Real, José T / Sanz, María J / Piqueras, Laura

Frontiers in endocrinology

2023 Volume 14, Page(s) 1154158

Abstract: Background/aims: Chemokines are known to play critical roles mediating inflammation in many pathophysiological processes. The aim of this study was to investigate the role of chemokine receptor CCR4 and its ligands CCL17 and CCL22 in human morbid ... ...

Abstract	Background/aims: Chemokines are known to play critical roles mediating inflammation in many pathophysiological processes. The aim of this study was to investigate the role of chemokine receptor CCR4 and its ligands CCL17 and CCL22 in human morbid obesity. Methods: Circulating levels of CCL17 and CCL22 were measured in 60 morbidly obese patients (mean age, 45 ± 1 years; body mass index/BMI, 44 ± 1 kg/m Results: Compared with controls, morbidly obese patients presented higher circulating levels of CCL17 (p=0.029) and CCL22 (p<0.001) and this increase was positively correlated with BMI (p=0.013 and p=0.0016), and HOMA-IR Index (p=0.042 and p< 0.001). Upregulation of CCR4, CCL17 and CCL22 expression was detected in VCAT in comparison with SCAT (p<0.05). Using the parallel-plate flow chamber model, blockade of endothelial CCR4 function with the neutralizing antibody anti-CCR4 in morbidly obese patients significantly reduced leucocyte adhesiveness to dysfunctional endothelium, a key event in atherogenesis. Additionally, CCL17 and CCL22 increased activation of the ERK1/2 mitogen-activated protein kinase signalling pathway in human aortic endothelial cells, which was significantly reduced by CCR4 inhibition (p=0.016 and p<0.05). Conclusion: Based on these findings, pharmacological modulation of the CCR4 axis could represent a new therapeutic approach to prevent adipose tissue dysfunction in obesity.
MeSH term(s)	Humans ; Adult ; Middle Aged ; Endothelial Cells/metabolism ; Obesity, Morbid/complications ; Obesity, Morbid/surgery ; Chemokine CCL17/genetics ; Chemokines ; Signal Transduction ; Receptors, Chemokine/metabolism ; Chemokine CCL22/genetics
Chemical Substances	Chemokine CCL17 ; Chemokines ; Receptors, Chemokine ; CCL17 protein, human ; CCL22 protein, human ; Chemokine CCL22
Language	English
Publishing date	2023-04-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1154158
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Article: Novel Therapies for Cardiometabolic Disease: Recent Findings in Studies with Hormone Peptide-Derived G Protein Coupled Receptor Agonists

Jiménez-Martí, Elena / Hurtado-Genovés, Gema / Aguilar-Ballester, María / Martínez-Hervás, Sergio / González-Navarro, Herminia

Nutrients. 2022 Sept. 13, v. 14, no. 18

2022

Abstract: The increasing prevalence of obesity and type 2 diabetes (T2DM) is provoking an important socioeconomic burden mainly in the form of cardiovascular disease (CVD). One successful strategy is the so-called metabolic surgery whose beneficial effects are ... ...

Abstract	The increasing prevalence of obesity and type 2 diabetes (T2DM) is provoking an important socioeconomic burden mainly in the form of cardiovascular disease (CVD). One successful strategy is the so-called metabolic surgery whose beneficial effects are beyond dietary restrictions and weight loss. One key underlying mechanism behind this surgery is the cooperative improved action of the preproglucagon-derived hormones, glucagon, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) which exert their functions through G protein-coupled receptors (GPCR). Great success has been reached with therapies based on the GLP-1 receptor monoagonism; therefore, a logical and rational approach is the use of the dual and triagonism of GCPC to achieve complete metabolic homeostasis. The present review describes novel findings regarding the complex biology of the preproglucagon-derived hormones, their signaling, and the drug development of their analogues, especially those acting as dual and triagonists. Moreover, the main investigations into animal models and ongoing clinical trials using these unimolecular dual and triagonists are included which have demonstrated their safety, efficacy, and beneficial effects on the CV system. These therapeutic strategies could greatly impact the treatment of CVD with unprecedented benefits which will be revealed in the next years.
Keywords	animals ; cardiovascular diseases ; drug development ; gastric inhibitory polypeptide ; glucagon ; glucagon-like peptide 1 ; homeostasis ; noninsulin-dependent diabetes mellitus ; obesity ; surgery ; weight loss
Language	English
Dates of publication	2022-0913
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14183775
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Article ; Online: Association of carotid atheroma plaque with IL-18 levels and with polymorphisms in the IL-18 receptor gene in a Mediterranean population.

Palanca, Ana / Bartual-Rodrigo, Amparo / Cuenca, Carolina / Mayo-López, Oscar D / Ampudia-Blasco, Francisco Javier / González-Navarro, Herminia / Ascaso, Juan F / García-García, Ana Bárbara / Chaves, Felipe Javier / Real, José T / Martínez-Hervás, Sergio

Clinica e investigacion en arteriosclerosis : publicacion oficial de la Sociedad Espanola de Arteriosclerosis

2024

Abstract: Background: Atherosclerosis is an inflammatory disease. Interleukin 18 (IL-18) is an inflammatory molecule that has been linked to the development of atherosclerosis and cardiovascular disease.: Objective: To evaluate the possible relationship ... ...

Title translation	Asociación de la placa de ateroma carotídea con los niveles plasmáticos de IL-18 y con polimorfismos en el gen del receptor de la IL-18 en la población mediterránea.
Abstract	Background: Atherosclerosis is an inflammatory disease. Interleukin 18 (IL-18) is an inflammatory molecule that has been linked to the development of atherosclerosis and cardiovascular disease. Objective: To evaluate the possible relationship between plasma levels of IL-18 and the presence of atherosclerosis evaluated at the carotid level, as well as to analyze the possible modulation by different polymorphisms in a Mediterranean population. Material and methods: Seven hundred and forty-six individuals from the metropolitan area of Valencia were included, recruited over a period of 2 years. Hydrocarbon and lipid metabolism parameters were determined using standard methodology and IL-18 using ELISA. In addition, carotid ultrasound was performed and the genotype of four SNPs related to the IL-18 signaling pathway was analyzed. Results: Patients with higher plasma levels of IL-18 had other associated cardiovascular risk factors. Elevated IL-18 levels were significantly associated with higher carotid IMT and the presence of atheromatous plaques. The genotype with the A allele of the SNP rs2287037 was associated with a higher prevalence of carotid atheromatous plaque. On the contrary, the genotype with the C allele of the SNP rs2293224 was associated with a lower prevalence of atheromatous plaque. Conclusions: High levels of IL-18 were significantly associated with a higher carotid IMT and the presence of atheromatous plaques, which appear to be influenced by genetic factors, as evidenced by associations between SNPs in the IL-18 receptor gene and the presence of atheroma plaque.
Language	Spanish
Publishing date	2024-01-11
Publishing country	Spain
Document type	Journal Article
ISSN	1578-1879
ISSN (online)	1578-1879
DOI	10.1016/j.arteri.2023.12.005
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Article ; Online: Anti-inflammatory Therapies for Cardiovascular Disease: Signaling Pathways and Mechanisms.

Martínez-Hervás, Sergio / González-Navarro, Herminia

Revista espanola de cardiologia (English ed.)

2019 Volume 72, Issue 9, Page(s) 767–773

Abstract: Cardiovascular diseases (CVD) are the clinical manifestation of atherosclerosis, a chronic inflammatory disease promoted by several risk factors such as dyslipidemia, type 2 diabetes mellitus, hypertension, and smoking. Acute CVD events are the result of ...

Abstract	Cardiovascular diseases (CVD) are the clinical manifestation of atherosclerosis, a chronic inflammatory disease promoted by several risk factors such as dyslipidemia, type 2 diabetes mellitus, hypertension, and smoking. Acute CVD events are the result of an unresolved inflammatory chronic state that promotes the rupture of unstable plaque lesions. Of note, the existing intensive therapies modify risk factors but do not prevent life-threatening recurrent ischemic events in high-risk patients, who have a residual inflammatory risk displayed by increased C-reactive protein (CRP) levels. Better understanding of the role of innate and adaptive immunity in plaque development and rupture has led to intensive investigation of anti-inflammatory strategies for CVD. Some of them are being tested in specific clinical trials and use lower doses of existing medications originally developed for other inflammatory diseases such as rheumatoid arthritis and psoriasis, which have high CVD risk. Other investigations are retrospective and meta-analyses of existing clinical trials that evaluate the incidence of CVD in these inflammatory diseases. Others are based on preclinical testing such as vaccines. In this article, we summarize the main anti-inflammatory strategies and associated molecular mechanisms that are being evaluated in preclinical or clinical CVD studies.
MeSH term(s)	Anti-Inflammatory Agents/therapeutic use ; Biomarkers/metabolism ; C-Reactive Protein/metabolism ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/prevention & control ; Humans ; Inflammation/drug therapy ; Inflammation/metabolism ; Signal Transduction
Chemical Substances	Anti-Inflammatory Agents ; Biomarkers ; C-Reactive Protein (9007-41-4)
Language	Spanish
Publishing date	2019-05-31
Publishing country	Spain
Document type	Journal Article ; Review
ISSN	1885-5857
ISSN (online)	1885-5857
DOI	10.1016/j.rec.2019.03.007
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Article ; Online: Light deficiency in Apoe-/-mice increases atheroma plaque size and vulnerability by modulating local immunity.

Hurtado-Genovés, Gema / Herrero-Cervera, Andrea / Vinué, Ángela / Martín-Vañó, Susana / Aguilar-Ballester, María / Taberner-Cortés, Alida / Jiménez-Martí, Elena / Martínez-Hervás, Sergio / González-Navarro, Herminia

Biochimica et biophysica acta. Molecular basis of disease

2024 Volume 1870, Issue 4, Page(s) 167052

Abstract: Previous research suggests a potential involvement of the cytokine LIGHT (TNFSF14) in atherosclerosis. In this study, the genetic inactivation of Light in Apolipoprotein E deficient mice (male and female C57BL) augmented plaque size and vulnerability ... ...

Abstract	Previous research suggests a potential involvement of the cytokine LIGHT (TNFSF14) in atherosclerosis. In this study, the genetic inactivation of Light in Apolipoprotein E deficient mice (male and female C57BL) augmented plaque size and vulnerability while decreasing Treg cells. Human and mouse transcriptomic results demonstrated deranged immune pathways in human atheromas with low LIGHT expression levels and in Light-deficient murine atheromas. In agreement with this, in vitro LIGHT-treatment of human lymphocytes, induced an elevation of Treg cell prevalence while proteomic analysis showed a downregulation of apoptotic and leukocyte cytotoxic pathways. Consistently, Light-deficient mouse lesions displayed increased plaque apoptosis and detrimental adventitial T-lymphocyte aggregates. Altogether suggested that LIGHT could promote a Treg prevalence in the local immunity to prevent the generation of vulnerable plaques via decreased cytotoxic microenvironment and apoptosis. Light gene delivery in Apoe-/-Light-/- mice, through bone marrow transplantation approaches, consistently diminished lesion size and restored local plaque immunity. Altogether demonstrate that Light-deficiency promotes atheroma plaque progression, at least in part through local loss of immune homeostasis and increased apoptosis. This study suggest that therapies based on the local delivery of LIGHT within plaques might therefore prevent immune cell derangement and advanced atherosclerosis.
MeSH term(s)	Animals ; Male ; Female ; Humans ; Mice ; Plaque, Atherosclerotic/metabolism ; Proteomics ; Mice, Inbred C57BL ; Atherosclerosis/metabolism ; Apolipoproteins E/genetics
Chemical Substances	Apolipoproteins E
Language	English
Publishing date	2024-02-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2024.167052
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Article: Understanding the Impact of Dietary Cholesterol on Chronic Metabolic Diseases through Studies in Rodent Models

Vinué, Ángela / Herrero-Cervera, Andrea / González-Navarro, Herminia

Nutrients. 2018 July 21, v. 10, no. 7

2018

Abstract: The development of certain chronic metabolic diseases has been attributed to elevated levels of dietary cholesterol. However, decades of research in animal models and humans have demonstrated a high complexity with respect to the impact of dietary ... ...

Abstract	The development of certain chronic metabolic diseases has been attributed to elevated levels of dietary cholesterol. However, decades of research in animal models and humans have demonstrated a high complexity with respect to the impact of dietary cholesterol on the progression of these diseases. Thus, recent investigations in non-alcoholic fatty liver disease (NAFLD) point to dietary cholesterol as a key factor for the activation of inflammatory pathways underlying the transition from NAFLD to non-alcoholic steatohepatitis (NASH) and to hepatic carcinoma. Dietary cholesterol was initially thought to be the key factor for cardiovascular disease development, but its impact on the disease depends partly on the capacity to modulate plasmatic circulating low-density lipoprotein (LDL) cholesterol levels. These studies evidence a complex relationship between these chronic metabolic diseases and dietary cholesterol, which, in certain conditions, might promote metabolic complications. In this review, we summarize rodent studies that evaluate the impact of dietary cholesterol on these two prevalent chronic diseases and their relevance to human pathology.
Keywords	animal models ; carcinoma ; cardiovascular diseases ; chronic diseases ; fatty liver ; humans ; low density lipoprotein cholesterol ; metabolic diseases ; rodents
Language	English
Dates of publication	2018-0721
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu10070939
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Article ; Online: Understanding the Impact of Dietary Cholesterol on Chronic Metabolic Diseases through Studies in Rodent Models.

Vinué, Ángela / Herrero-Cervera, Andrea / González-Navarro, Herminia

Nutrients

2018 Volume 10, Issue 7

Abstract	The development of certain chronic metabolic diseases has been attributed to elevated levels of dietary cholesterol. However, decades of research in animal models and humans have demonstrated a high complexity with respect to the impact of dietary cholesterol on the progression of these diseases. Thus, recent investigations in non-alcoholic fatty liver disease (NAFLD) point to dietary cholesterol as a key factor for the activation of inflammatory pathways underlying the transition from NAFLD to non-alcoholic steatohepatitis (NASH) and to hepatic carcinoma. Dietary cholesterol was initially thought to be the key factor for cardiovascular disease development, but its impact on the disease depends partly on the capacity to modulate plasmatic circulating low-density lipoprotein (LDL) cholesterol levels. These studies evidence a complex relationship between these chronic metabolic diseases and dietary cholesterol, which, in certain conditions, might promote metabolic complications. In this review, we summarize rodent studies that evaluate the impact of dietary cholesterol on these two prevalent chronic diseases and their relevance to human pathology.
MeSH term(s)	Animals ; Atherosclerosis/etiology ; Cholesterol, Dietary/adverse effects ; Disease Models, Animal ; Metabolic Diseases/complications ; Non-alcoholic Fatty Liver Disease/etiology
Chemical Substances	Cholesterol, Dietary
Language	English
Publishing date	2018-07-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu10070939
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Article ; Online: Novel Therapies for Cardiometabolic Disease: Recent Findings in Studies with Hormone Peptide-Derived G Protein Coupled Receptor Agonists.

Jiménez-Martí, Elena / Hurtado-Genovés, Gema / Aguilar-Ballester, María / Martínez-Hervás, Sergio / González-Navarro, Herminia

Nutrients

2022 Volume 14, Issue 18

Abstract	The increasing prevalence of obesity and type 2 diabetes (T2DM) is provoking an important socioeconomic burden mainly in the form of cardiovascular disease (CVD). One successful strategy is the so-called metabolic surgery whose beneficial effects are beyond dietary restrictions and weight loss. One key underlying mechanism behind this surgery is the cooperative improved action of the preproglucagon-derived hormones, glucagon, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) which exert their functions through G protein-coupled receptors (GPCR). Great success has been reached with therapies based on the GLP-1 receptor monoagonism; therefore, a logical and rational approach is the use of the dual and triagonism of GCPC to achieve complete metabolic homeostasis. The present review describes novel findings regarding the complex biology of the preproglucagon-derived hormones, their signaling, and the drug development of their analogues, especially those acting as dual and triagonists. Moreover, the main investigations into animal models and ongoing clinical trials using these unimolecular dual and triagonists are included which have demonstrated their safety, efficacy, and beneficial effects on the CV system. These therapeutic strategies could greatly impact the treatment of CVD with unprecedented benefits which will be revealed in the next years.
MeSH term(s)	Animals ; Cardiovascular Diseases/drug therapy ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Gastric Inhibitory Polypeptide/metabolism ; Gastric Inhibitory Polypeptide/therapeutic use ; Glucagon ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucose/therapeutic use ; Incretins ; Peptides/pharmacology ; Peptides/therapeutic use ; Proglucagon
Chemical Substances	Glucagon-Like Peptide-1 Receptor ; Incretins ; Peptides ; Proglucagon (55963-74-1) ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-09-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14183775
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Article ; Online: Glucose and Insulin Tolerance Tests in the Mouse.

Vinué, Ángela / González-Navarro, Herminia

Methods in molecular biology (Clifton, N.J.)

2015 Volume 1339, Page(s) 247–254

Abstract: In vivo metabolic tests are highly valuable to determine whether atherosclerosis progression in mouse models is accompanied by carbohydrate metabolism alterations such as glucose intolerance and insulin resistance. In this chapter, we describe protocols ... ...

Abstract	In vivo metabolic tests are highly valuable to determine whether atherosclerosis progression in mouse models is accompanied by carbohydrate metabolism alterations such as glucose intolerance and insulin resistance. In this chapter, we describe protocols to perform in the mouse glucose and insulin tolerance tests, two metabolic assays which evaluate the glucose tolerance and the insulin sensitivity, respectively.
MeSH term(s)	Animals ; Atherosclerosis/blood ; Atherosclerosis/complications ; Atherosclerosis/physiopathology ; Biomarkers/blood ; Blood Glucose/metabolism ; Disease Models, Animal ; Disease Progression ; Female ; Glucose Intolerance/blood ; Glucose Intolerance/diagnosis ; Glucose Intolerance/etiology ; Glucose Intolerance/physiopathology ; Glucose Tolerance Test/methods ; Insulin/blood ; Insulin Resistance ; Male ; Mice ; Predictive Value of Tests ; Reproducibility of Results ; Time Factors
Chemical Substances	Biomarkers ; Blood Glucose ; Insulin
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-2929-0_17
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Article ; Online: Impact of Cholesterol Metabolism in Immune Cell Function and Atherosclerosis.

Aguilar-Ballester, María / Herrero-Cervera, Andrea / Vinué, Ángela / Martínez-Hervás, Sergio / González-Navarro, Herminia

Nutrients

2020 Volume 12, Issue 7

Abstract: Cholesterol, the most important sterol in mammals, helps maintain plasma membrane fluidity and is a precursor of bile acids, oxysterols, and steroid hormones. Cholesterol in the body is obtained from the diet or can be de novo synthetized. Cholesterol ... ...

Abstract	Cholesterol, the most important sterol in mammals, helps maintain plasma membrane fluidity and is a precursor of bile acids, oxysterols, and steroid hormones. Cholesterol in the body is obtained from the diet or can be de novo synthetized. Cholesterol homeostasis is mainly regulated by the liver, where cholesterol is packed in lipoproteins for transport through a tightly regulated process. Changes in circulating lipoprotein cholesterol levels lead to atherosclerosis development, which is initiated by an accumulation of modified lipoproteins in the subendothelial space; this induces significant changes in immune cell differentiation and function. Beyond lesions, cholesterol levels also play important roles in immune cells such as monocyte priming, neutrophil activation, hematopoietic stem cell mobilization, and enhanced T cell production. In addition, changes in cholesterol intracellular metabolic enzymes or transporters in immune cells affect their signaling and phenotype differentiation, which can impact on atherosclerosis development. In this review, we describe the main regulatory pathways and mechanisms of cholesterol metabolism and how these affect immune cell generation, proliferation, activation, and signaling in the context of atherosclerosis.
MeSH term(s)	Animals ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Cell Proliferation ; Cholesterol/blood ; Cholesterol/metabolism ; Hematopoiesis ; Homeostasis ; Humans ; Immunity, Cellular ; Lipid Metabolism ; Lipoproteins/metabolism ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Monocytes/metabolism ; Neutrophils/metabolism ; T-Lymphocytes/metabolism
Chemical Substances	Lipoproteins ; lipoprotein cholesterol ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2020-07-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12072021
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