4.3 Article

Guanidino Compounds as Cause of Cardiovascular Damage in Chronic Kidney Disease: An in vitro Evaluation

期刊

BLOOD PURIFICATION
卷 30, 期 4, 页码 277-287

出版社

KARGER
DOI: 10.1159/000320765

关键词

Atherosclerosis; Chronic kidney disease; Guanidino compounds; SDMA; Uremic toxins; Vascular damage

向作者/读者索取更多资源

Chronic kidney disease is considered a major cause of cardiovascular risk and non-traditional risk factors remain largely unknown. The in vitro toxicity of 10 guanidino compounds (GCs) was evaluated via a standardized approach on different cell systems of relevance in cardiovascular disease. The parameters evaluated were production of reactive oxygen species, expression of surface molecules, cell proliferation, cytotoxicity and calcification. Several GCs had a stimulatory effect on monocytes and granulocytes (SDMA, creatine and guanidinobutyric acid (GBA)). Some GCs (guandine (G), guanidinosuccinic acid (GSA) and SDMA) inhibited endothelial cell proliferation or reduced calcification in osteoblast-like human VSMC (ADMA, GSA and SDMA). Stimulation of osteoclastogenesis could be demonstrated for ADMA, G, guanidinoacetic acid and GBA in a RAW264.7 cell line. No compounds were cytotoxic to AoSMC or endothelial cells, nor influenced their viability. GCs, especially SDMA, likely contribute to cardiovascular complications in uremia, mainly those related to microinflammation and leukocyte activation. Copyright (C) 2010 S. Karger AG, Basel

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.3
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Cardiac & Cardiovascular Systems

Vitamin D3 Supplementation Alleviates Left Ventricular Dysfunction in a Mouse Model of Diet-Induced Type 2 Diabetes: Potential Involvement of Cardiac Lipotoxicity Modulation

Clothilde Philouze, Jean-Charles Martin, Catherine Riva, Alexandra Marziou, Catherine Defoort, Charlene Couturier, Thierry Berton, Julien Astier, Bernard Jover, Nathalie Gayrard, Cyril Reboul, Sandrine Gayrard, Jean-Francois Landrier, Philippe Obert

Summary: Vitamin D-3 supplementation did not affect glucose homeostasis, but improved cardiac remodeling and regional myocardial function, reducing levels of ceramides and diacylglycerol in the myocardium. This study demonstrated the potential benefits of vitamin D in diabetic cardiac disease.

CARDIOVASCULAR DRUGS AND THERAPY (2022)

Review Biochemistry & Molecular Biology

Renal insufficiency and chronic kidney disease - Promotor or consequence of pathological post-translational modifications

Jonas Laget, Flore Duranton, Angel Argiles, Nathalie Gayrard

Summary: This review article discusses the interconnections between chronic kidney disease (CKD) and protein post-translational modifications (PTMs), highlighting the role of PTMs in CKD pathophysiology and kidney damage.

MOLECULAR ASPECTS OF MEDICINE (2022)

Article Transplantation

Neutrophil:lymphocyte ratio correlates with the uremic toxin indoxyl sulfate and predicts the risk of death in patients on hemodialysis

Guillaume Lano, Marion Sallee, Marion Pelletier, Stanislas Bataille, Megan Fraisse, Nathalie McKay, Philippe Brunet, Laetitia Dou, Stephane Burtey

Summary: This study found that the neutrophil:lymphocyte ratio (NLR) can predict mortality and cardiovascular events in hemodialysis (HD) patients, and it is positively correlated with the level of the uremic toxin indoxyl sulfate (IS).

NEPHROLOGY DIALYSIS TRANSPLANTATION (2022)

Article Transplantation

Mechanisms of myostatin and activin A accumulation in chronic kidney disease

Stanislas Bataille, Laetitia Dou, Marc Bartoli, Marion Sallee, Julien Aniort, Borhane Ferkak, Rania Chermiti, Nathalie McKay, Nathalie Da Silva, Stephane Burtey, Stephane Poitevin

Summary: In chronic kidney disease (CKD), the plasma concentrations of myostatin and activin A are increased, possibly due to reduced renal clearance. Furthermore, we observed increased production of activin A in the kidney and heart, which may be related to muscle wasting. Therefore, myostatin and activin A should be added to the list of uremic toxins.

NEPHROLOGY DIALYSIS TRANSPLANTATION (2022)

Article Dermatology

CD146 at the Interface between Oxidative Stress and the Wnt Signaling Pathway in Systemic Sclerosis

Xavier Heim, Julien Bermudez, Ahmad Joshkon, Elise Kaspi, Richard Bachelier, Marie Nollet, Melanie Velier, Laetitia Dou, Alexandre Brodovitch, Alexandrine Foucault-Bertaud, Aurelie S. Leroyer, Audrey Benyamine, Aurelie Daumas, Brigitte Granel, Florence Sabatier, Francoise Dignat-George, Marcel Blot-Chabaud, Nathalie Bardin

Summary: This study reveals the involvement of CD146 in the regulation of Wnt/ROS signaling in skin fibrosis of systemic sclerosis. The absence of CD146 leads to procanonical Wnt signaling, increased ROS content, and DNA oxidative damage. Furthermore, CD146 and its ligand are upregulated in fibroblasts from patients with systemic sclerosis. These findings highlight the importance of CD146 in the pathogenesis of systemic sclerosis and provide insights for innovative therapeutic strategies.

JOURNAL OF INVESTIGATIVE DERMATOLOGY (2022)

Article Multidisciplinary Sciences

Vascular calcification in different arterial beds in ex vivo ring culture and in vivo rat model

Karen Muyor, Jonas Laget, Irene Cortijo, Flore Duranton, Bernard Jover, Angel Argiles, Nathalie Gayrard

Summary: Vascular calcification is a risk factor for cardiovascular and kidney diseases. The anatomical distribution of vascular calcifications on different arteries and artery locations was mapped in cultured artery rings (ex vivo) and in a rat model of elastocalcinosis (in vivo). The study showed that arterial calcification increased with narrowing of vessels and was accompanied by fibrosis and apoptosis. These differences represent the local susceptibility of the vessels to the calcifying processes.

SCIENTIFIC REPORTS (2022)

Article Food Science & Technology

Protein/Fiber Index Modulates Uremic Toxin Concentrations in Hemodialysis Patients

Manon Ebersolt, Tacy Santana Machado, Cecilia Mallmann, Nathalie Mc-Kay, Laetitia Dou, Dammar Bouchouareb, Philippe Brunet, Stephane Burtey, Marion Sallee

Summary: A low protein/fiber index is associated with lower concentrations of uremic toxins in anuric hemodialysis patients. Diets with increased fiber intake should be tested to determine if they can reduce serum concentrations of p-cresyl sulfate and indoxyl sulfate.

TOXINS (2022)

Review Food Science & Technology

Gut-Kidney Axis Investigations in Animal Models of Chronic Kidney Disease

Piotr Bartochowski, Nathalie Gayrard, Stephanie Bornes, Celine Druart, Angel Argiles, Magali Cordaillat-Simmons, Flore Duranton

Summary: Chronic kidney disease affects the gut microbiota, and animal models can be used to study the gut-kidney axis. Murine models replicate the symptoms of chronic kidney disease, including slowed gut transit and altered intestinal barrier function.

TOXINS (2022)

Article Biochemistry & Molecular Biology

Systematic Comparison of Uremic Toxin Removal Using Different Hemodialysis Modes: A Single-Center Crossover Prospective Observational Study

Ariane Duval-Sabatier, Stephane Burtey, Marion Pelletier, Manon Laforet, Laetitia Dou, Marion Sallee, Anne-Marie Lorec, Hafssa Knidiri, Floriane Darbon, Yvon Berland, Philippe Brunet

Summary: Hemodialysis can reduce uremic toxins, and hemodiafiltration improves the removal of middle molecules. However, it has no effect on indoles concentration, and different treatment methods do not significantly differ in the removal of protein-bound solutes.

BIOMEDICINES (2023)

Article Cell Biology

Cardiac remodeling associated with chronic kidney disease is enhanced in a rat model of metabolic syndrome: Preparation of mesenchymal transition

Maelle Plawecki, Nathalie Gayrard, Laura Jeanson, Anthony Chauvin, Anne-Dominique Lajoix, Jean-Paul Cristol, Bernard Jover, Fabrice Raynaud

Summary: Cardiac alteration due to chronic kidney disease is accompanied by tissue fibrosis, which involves myofibroblasts and endothelial to mesenchymal transitions. Additionally, obesity and insulin resistance exacerbate cardiovascular risk in chronic kidney disease (CKD). This study aimed to investigate how pre-existing metabolic disease and endothelial to mesenchymal transition contribute to cardiac fibrosis in CKD. Rats fed a cafeteria diet were found to be obese, hypertensive, and insulin resistant. CKD rats exhibited high levels of cardiac fibrosis, with collagen-1 and nestin expressions increased regardless of diet. Interestingly, rats with CKD and a cafeteria diet showed an increase in CD31 and alpha-SMA co-staining, suggesting the involvement of endothelial to mesenchymal transition in cardiac fibrosis.

MOLECULAR AND CELLULAR BIOCHEMISTRY (2023)

Article Transplantation

Indoxyl sulfate inhibits muscle cell differentiation via Myf6/MRF4 and MYH2 downregulation

Stanislas Bataille, Nathalie McKay, Laetitia Koppe, Alice Beau, Berengere Benoit, Marc Bartoli, Nathalie Da Silva, Stephane Poitevin, Julien Aniort, Rania Chermiti, Stephane Burtey, Laetitia Dou

Summary: Indoxyl sulfate (IS), an indolic uremic toxin, inhibits the expression of Myf6/MRF4 and MYH2 during muscle cell differentiation, leading to a defect in myotube structure. This provides new insights into the role of IS in muscle atrophy observed in CKD.

NEPHROLOGY DIALYSIS TRANSPLANTATION (2023)

Article Cell Biology

Implications of Senescent Cell Burden and NRF2 Pathway in Uremic Calcification: A Translational Study

Jonas Laget, Sam Hobson, Karen Muyor, Flore Duranton, Irene Cortijo, Piotr Bartochowski, Bernard Jover, Anne-Dominique Lajoix, Magnus Soderberg, Thomas Ebert, Peter Stenvinkel, Angel Argiles, Karolina Kublickiene, Nathalie Gayrard

Summary: Increased senescent cell burden and dysregulation of the NRF2 pathway play a role in vascular calcification. In vivo and in vitro studies showed increased senescence markers in calcified tissues and VSMCs exposed to uremic serum. NRF2 expression correlated with calcification in vivo but was depleted in vitro. These findings highlight the therapeutic potential of targeting senescence and the NRF2 pathway in the treatment of VC in CKD.
Article Nutrition & Dietetics

Cafeteria Diet-Induced Obesity Worsens Experimental CKD

Jonas Laget, Irene Cortijo, Juliana H. H. Boukhaled, Karen Muyor, Flore Duranton, Bernard Jover, Fabrice Raynaud, Anne-Dominique Lajoix, Angel Argiles, Nathalie Gayrard

Summary: Obesity exacerbates renal inflammation and fibrosis in chronic kidney disease (CKD). Certain substances such as interleukin 11, dipeptidyl peptidase 4, and serpin 1 may directly affect the process of fibrosis.

NUTRIENTS (2023)

Meeting Abstract Cardiac & Cardiovascular Systems

CHARACTERIZATION OF MEDIATORS OF VASCULAR CALCIFICATION DERIVED FROM ADRENAL GLANDS

S. Bhargava, J. Jankowski, S. Orth-Alampour, N. Gayrard, A. Argiles

ATHEROSCLEROSIS (2022)

暂无数据