RESUMEN
Lipidome perturbation occurring during meta-inflammation is associated to left ventricle (LV) remodeling though the activation of the NLRP3 inflammasome, a key regulator of chronic inflammation in obesity-related disorders. Little is known about phosphatidylcholine (PC) and phosphatidylethanolamine (PE) as DAMP-induced NLRP3 inflammasome. Our study is aimed to evaluate if a systemic reduction of PC/PE molar ratio can affect NLRP3 plasma levels in cardiovascular disease (CVD) patients with insulin resistance (IR) risk. Forty patients from IRCCS Policlinico San Donato were enrolled, and their blood samples were drawn before heart surgery. LV geometry measurements were evaluated by echocardiography and clinical data associated to IR risk were collected. PC and PE were quantified by ESI-MS/MS. Circulating NLRP3 was quantified by an ELISA assay. Our results have shown that CVD patients with IR risk presented systemic lipid impairment of PC and PE species and their ratio in plasma was inversely associated to NLRP3 levels. Interestingly, CVD patients with IR risk presented LV changes directly associated to increased levels of NLRP3 and a decrease in PC/PE ratio in plasma, highlighting the systemic effect of meta-inflammation in cardiac response. In summary, PC and PE can be considered bioactive mediators associated to both the NLRP3 and LV changes in CVD patients with IR risk.
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Enfermedades Cardiovasculares , Inflamasomas , Resistencia a la Insulina , Proteína con Dominio Pirina 3 de la Familia NLR , Fosfatidilcolinas , Fosfatidiletanolaminas , Remodelación Ventricular , Humanos , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Fosfatidilcolinas/sangre , Inflamasomas/metabolismo , Masculino , Femenino , Persona de Mediana Edad , Fosfatidiletanolaminas/sangre , Fosfatidiletanolaminas/metabolismo , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/patología , AncianoRESUMEN
Inflammation is the primary response of different disorders, and these encompass a wide range of conditions in various tissues and organs [...].
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Biomarcadores , Inflamación , Humanos , Inflamación/metabolismo , Biomarcadores/metabolismo , AnimalesRESUMEN
Obesity is an epidemic condition linked to cardiovascular disease severity and mortality. Fat localization and type represent cardiovascular risk estimators. Importantly, visceral fat secretes adipokines known to promote low-grade inflammation that, in turn, modulate its secretome and cardiac metabolism. In this regard, IL-33 regulates the functions of various immune cells through ST2 binding and-following its role as an immune sensor to infection and stress-is involved in the pro-fibrotic remodeling of the myocardium. Here we further investigated the IL-33/ST2 effects on cardiac remodeling in obesity, focusing on molecular pathways linking adipose-derived IL-33 to the development of fibrosis or hypertrophy. We analyzed the Zucker Fatty rat model, and we developed in vitro models to mimic the adipose and myocardial relationship. We demonstrated a dysregulation of IL-33/ST2 signaling in both adipose and cardiac tissue, where they affected Epac proteins and myocardial gene expression, linked to pro-fibrotic signatures. In Zucker rats, pro-fibrotic effects were counteracted by ghrelin-induced IL-33 secretion, whose release influenced transcription factor expression and ST2 isoforms balance regulation. Finally, the effect of IL-33 signaling is dependent on several factors, such as cell types' origin and the balancing of ST2 isoforms. Noteworthy, it is reasonable to state that considering IL-33 to have a unique protective role should be considered over-simplistic.
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Interleucina-33 , Obesidad , Receptores de Interleucina-1 , Remodelación Ventricular , Animales , Ratas , Cardiomegalia/genética , Cardiomegalia/metabolismo , Modelos Animales de Enfermedad , Fibrosis/genética , Fibrosis/metabolismo , Ghrelina/genética , Ghrelina/metabolismo , Factores de Intercambio de Guanina Nucleótido/genética , Factores de Intercambio de Guanina Nucleótido/metabolismo , Proteína 1 Similar al Receptor de Interleucina-1/genética , Proteína 1 Similar al Receptor de Interleucina-1/metabolismo , Interleucina-33/genética , Interleucina-33/metabolismo , Miocardio/metabolismo , Obesidad/complicaciones , Obesidad/genética , Obesidad/metabolismo , Ratas Zucker , Receptores de Interleucina-1/genética , Receptores de Interleucina-1/metabolismo , Remodelación Ventricular/genética , Remodelación Ventricular/fisiologíaRESUMEN
The etiopathogenesis of obesity-related chronic kidney disease (CKD) is still scarcely understood. To this aim, we assessed the effect of high-fat diet (HF) on molecular pathways leading to organ damage, steatosis, and fibrosis. Six-week-old male C57BL/6N mice were fed HF diet or normal chow for 20 weeks. Kidneys were collected for genomic, proteomic, histological studies, and lipid quantification. The main findings were as follows: (1) HF diet activated specific pathways leading to fibrosis and increased fatty acid metabolism; (2) HF diet promoted a metabolic shift of lipid metabolism from peroxisomes to mitochondria; (3) no signs of lipid accumulation and/or fibrosis were observed, histologically; (4) the early signs of kidney damage seemed to be related to changes in membrane protein expression; (5) the proto-oncogene MYC was one of the upstream transcriptional regulators of changes occurring in protein expression. These results demonstrated the potential usefulness of specific selected molecules as early markers of renal injury in HF, while histomorphological changes become visible later in obesity-related CDK. The integration of these information with data from biological fluids could help the identification of biomarkers useful for the early detection and prevention of tissue damage in clinical practice.
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Dieta Alta en Grasa , Insuficiencia Renal Crónica , Animales , Biomarcadores/metabolismo , Dieta Alta en Grasa/efectos adversos , Fibrosis , Riñón/metabolismo , Lípidos , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Obesidad/metabolismo , Proteoma/metabolismo , Proteómica , Insuficiencia Renal Crónica/metabolismoRESUMEN
BACKGROUND AND AIMS: Magnesium is a fundamental cation that regulates neuronal transmission, protein synthesis, energy metabolism. Magnesium deficiency mostly affects nervous and cardiovascular systems determining weakness, tremors, seizure and arrhythmias. This condition retains also a role in memory function and neuronal plasticity. Importantly magnesium deficiency could remain latent and asymptomatic resulting a risk factor for cardiovascular disease. In this sense we aim to determine magnesium status in patient presenting cognitive impairment of vascular origin. METHODS: 21 healthy subjects and 27 patients presenting vascular cognitive impairment were included in this study. Both plasma and intraerythrocitary magnesium level were measured to detect magnesium deficiency and cognitive performance was evaluated trough Mini Mental State Evaluation (MMSE). RESULTS: Here we showed that patients presenting vascular cognitive impairment present intraerythrocitary magnesium level lower than age-matched healthy subjects. To note their plasma magnesium resulted within reference limit. CONCLUSION: We suggest that intracellular magnesium laboratory measurement is needed to detect occult magnesium deficiency in population at risk. Magnesium supplementation could represent an adjuvant for healthy aging in high risk population.
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Disfunción Cognitiva , Deficiencia de Magnesio , Enfermedades Vasculares , Disfunción Cognitiva/complicaciones , Eritrocitos , Humanos , Deficiencia de Magnesio/complicaciones , Proyectos PilotoRESUMEN
Epicardial adipose tissue (EAT) has the unique property to release mediators that nourish the heart in healthy conditions, an effect that becomes detrimental when volume expands and proinflammatory cytokines start to be produced. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a proinflammatory mediator involved in atherosclerosis, is also produced by visceral fat. Due to the correlation of inflammation with PCSK9 and EAT enlargement, we evaluated whether PCSK9 was expressed in EAT and associated with EAT inflammation and volume. EAT samples were isolated during surgery. EAT thickness was measured by echocardiography. A microarray was used to explore EAT transcriptoma. The PCSK9 protein levels were measured by Western Blot in EAT and ELISA in plasma. PCSK9 was expressed at both the gene and protein levels in EAT. We found a positive association with EAT thickness and local proinflammatory mediators, in particular, chemokines for monocytes and lymphocytes. No association was found with the circulating PCSK9 level. The expression of PCSK9 in EAT argues that PCSK9 is part of the EAT secretome and EAT inflammation is associated with local PCSK9 expression, regardless of circulating PCSK9 levels. Whether reducing EAT inflammation or PCSK9 local levels may have beneficial effects on EAT metabolism and cardiovascular risk needs further investigations.
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Tejido Adiposo/metabolismo , Inflamación/metabolismo , Pericardio/metabolismo , Proproteína Convertasa 9/metabolismo , Anciano , Antropometría , Índice de Masa Corporal , Estudios de Casos y Controles , Quimiocinas/metabolismo , Enfermedad de la Arteria Coronaria/complicaciones , Femenino , Enfermedades de las Válvulas Cardíacas/complicaciones , Humanos , Linfocitos/metabolismo , Masculino , Persona de Mediana Edad , Monocitos/metabolismo , Análisis por Matrices de Proteínas , RiesgoRESUMEN
Osteopontin (OPN) is a multifaceted matricellular protein, with well-recognized roles in both the physiological and pathological processes in the body. OPN is expressed in the main organs and cell types, in which it induces different biological actions. During physiological conditioning, OPN acts as both an intracellular protein and soluble excreted cytokine, regulating tissue remodeling and immune-infiltrate in adipose tissue the heart and the kidney. In contrast, the increased expression of OPN has been correlated with the severity of the cardiovascular and renal outcomes associated with obesity. Indeed, OPN expression is at the "cross roads" of visceral fat extension, cardiovascular diseases (CVDs) and renal disorders, in which OPN orchestrates the molecular interactions, leading to chronic low-grade inflammation. The common factor associated with OPN overexpression in adipose, cardiac and renal tissues seems attributable to the concomitant increase in visceral fat size and the increase in infiltrated OPN+ macrophages. This review underlines the current knowledge on the molecular interactions between obesity and the cardiac-renal disorders ruled by OPN.
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Cardiopatías/genética , Enfermedades Renales/genética , Miocardio/metabolismo , Osteopontina/genética , Tejido Adiposo/metabolismo , Cardiopatías/metabolismo , Cardiopatías/patología , Humanos , Inflamación/genética , Inflamación/patología , Resistencia a la Insulina/genética , Grasa Intraabdominal/metabolismo , Riñón/metabolismo , Riñón/patología , Enfermedades Renales/metabolismo , Enfermedades Renales/patología , Miocardio/patología , Obesidad/genética , Obesidad/metabolismo , Obesidad/patología , Osteopontina/metabolismoRESUMEN
There is recent evidence that the dysfunctional responses of a peculiar visceral fat deposit known as epicardial adipose tissue (EAT) can directly promote cardiac enlargement in the case of obesity. Here, we observed a newer molecular pattern associated with LV dysfunction mediated by prostaglandin E2 (PGE2) deregulation in EAT in a cardiovascular disease (CVD) population. A series of 33 overweight CVD males were enrolled and their EAT thickness, LV mass, and volumes were measured by echocardiography. Blood, plasma, EAT, and SAT biopsies were collected for molecular and proteomic assays. Our data show that PGE2 biosynthetic enzyme (PTGES-2) correlates with echocardiographic parameters of LV enlargement: LV diameters, LV end diastolic volume, and LV masses. Moreover, PTGES-2 is directly associated with EPAC2 gene (r = 0.70, p < 0.0001), known as a molecular inducer of ST2/IL-33 mediators involved in maladaptive heart remodelling. Furthermore, PGE2 receptor 3 (PTEGER3) results are downregulated and its expression is inversely associated with ST2/IL-33 expression. Contrarily, PGE2 receptor 4 (PTGER4) is upregulated in EAT and directly correlates with ST2 molecular expression. Our data suggest that excessive body fatness can shift the EAT transcriptome to a pro-tissue remodelling profile, may be driven by PGE2 deregulation, with consequent promotion of EPAC2 and ST2 signalling.
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Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/metabolismo , Dinoprostona/metabolismo , Factores de Intercambio de Guanina Nucleótido/metabolismo , Proteína 1 Similar al Receptor de Interleucina-1/metabolismo , Pericardio/patología , Transducción de Señal , Remodelación Ventricular , Adiposidad , Anciano , Anciano de 80 o más Años , Biomarcadores , Pesos y Medidas Corporales , Enfermedades Cardiovasculares/diagnóstico , Ecocardiografía , Pruebas de Función Cardíaca , Humanos , Persona de Mediana Edad , Sobrepeso/complicaciones , Sobrepeso/metabolismo , Prostaglandina-E Sintasas/genética , Prostaglandina-E Sintasas/metabolismo , Subtipo EP3 de Receptores de Prostaglandina E/genética , Subtipo EP3 de Receptores de Prostaglandina E/metabolismoRESUMEN
AIMS: Genetic and environmental factors all interact in the risk of progression of valvular dysfunctions. Previous studies reported a relation between valve diseases and epicardial adipose tissue (EAT) thickness. The aim of this study was to verify the possible relationship between the molecular pattern of EAT related to IL-13 fibrogenic cytokine expression and valve dysfunction. METHODS AND RESULTS: A valvular heart disease (VHD) population was stratified according to their median EAT thickness (7â¯mm). The molecular expression of IL-13 in EAT is directly related to the molecular expression of genes associated with extracellular matrix (ECM) turnover, macrophage infiltration and promotion of the formation of ectopic calcific nodules involved in aorta coarctation and calcification. CONCLUSION: IL-13 gene expression in altered EAT is directly related to the expression of genes involved in ECM turnover and the formation of ectopic calcific nodules, suggesting measurements of EAT as a stratification risk factor for valve instability in the VHD patients.
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Tejido Adiposo/patología , Calcinosis/patología , Enfermedades de las Válvulas Cardíacas/patología , Interleucina-13/metabolismo , Pericardio/patología , Anciano , Calcinosis/metabolismo , Progresión de la Enfermedad , Mapeo Epicárdico , Femenino , Enfermedades de las Válvulas Cardíacas/etiología , Enfermedades de las Válvulas Cardíacas/metabolismo , Humanos , Interleucina-13/genética , Masculino , Persona de Mediana Edad , Factores de Riesgo , Transducción de SeñalRESUMEN
OBJECTIVES: Cognitive and mood changes can affect postoperative recovery in hospitalized older adults undergoing major surgical procedures, but few studies have considered postoperative cognitive interventions to sustain such patients' cognitive functioning and mood. The aim of this pilot study was to assess the efficacy of working memory training in improving cognitive functioning and mood, or emotional functioning, in older adults undergoing major surgery. METHODS: Thirty-four older adults (from 64 to 75 years of age) hospitalized for partial or total arthroplasty of the knee were randomly assigned to either a trained group (Nâ¯=â¯18) or an active control group (Nâ¯=â¯16). The former received working memory training during the postoperative period, while the latter engaged in alternative activities. In addition to specific training gains in a working memory task similar to the one used in the training (criterion task), transfer effects to cognitive abilities (short- and long-term memory, and cognitive inhibition), and mood or emotional functioning (signs of depression or anxiety) were investigated. RESULTS: Immediately after the training, results showed a main effect of group (in favor of the trained group) in the criterion task, in one of the short-term memory measures, and in cognitive inhibition. In addition, only the trained group showed a decrease in depression and anxiety scores. CONCLUSION: The results of this pilot study suggest that cognitive training targeting working memory administered in the postoperative period after major surgery can sustain older adults' cognitive and emotional functioning, and especially their mood.
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Envejecimiento/psicología , Artroplastia de Reemplazo de Rodilla/psicología , Memoria a Corto Plazo , Anciano , Cognición , Emociones , Femenino , Humanos , Italia , Aprendizaje , Masculino , Proyectos Piloto , Transferencia de Experiencia en PsicologíaRESUMEN
Most of the obesity-related complications are due to ectopic fat accumulation. Recently, the activation of the cell-surface receptor for advanced glycation end products (RAGE) has been associated with lipid accumulation in different organs. Nevertheless, the role of RAGE and sRAGE, the soluble form that prevents ligands to activate RAGE, in intramyocardial lipid accumulation is presently unknown. To this aim, we analyzed whether, in obesity, intramyocardial lipid accumulation and lipid metabolism-related transcriptome are related to RAGE and sRAGE. Heart and serum samples were collected from 10 lean (L) and 10 obese (OB) Zucker rats. Oil red staining was used to detect lipids on frozen heart sections. The lipid metabolism-related transcriptome (84 genes) was analyzed by a specific PCR array. Heart RAGE expression was explored by real-time RT-PCR and Western blot analyses. Serum levels of sRAGE (total and endogenous secretory form (esRAGE)) were quantified by ELISA. Genes promoting fatty acid transport, activation, and oxidation in mitochondria/peroxisomes were upregulated in OB hearts. Intramyocardial lipid content did not differ between OB and L rats, as well as RAGE expression. A slight increase in epicardial adipose tissue was observed in OB hearts. Total sRAGE and esRAGE concentrations were significantly higher in OB rats. sRAGE may protect against obesity-induced intramyocardial lipid accumulation by preventing RAGE hyperexpression, therefore allowing lipids to be metabolized. EAT also played a protective role by working as a buffering system that protects the myocardium against exposure to excessively high levels of fatty acids. These observations reinforce the potential role of RAGE pathway as an interesting therapeutic target for obesity-related complications, at least at the cardiovascular level.
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Productos Finales de Glicación Avanzada/metabolismo , Metabolismo de los Lípidos/fisiología , Miocardio/metabolismo , Obesidad/metabolismo , Receptor para Productos Finales de Glicación Avanzada/metabolismo , Animales , Biomarcadores , Western Blotting , Ensayo de Inmunoadsorción Enzimática , Lípidos , Masculino , Obesidad/sangre , Ratas , Ratas Zucker , Reacción en Cadena en Tiempo Real de la PolimerasaRESUMEN
End-stage renal disease patients on dialysis (CKD-G5D) have a high mortality rate due to cardiovascular diseases (CVD). In these patients, inflammation, oxidative stress, and uremia increase the production of glycation products (AGEs) which in turn accelerate CVD onset and progression. Recently, attention has been given to the soluble receptor for AGEs (sRAGE) as a marker of inflammation, oxidative stress, atherosclerosis, and heart failure in CKD-G5D. However, its association with patient outcomes is still under debate. Our aim is to explore whether sRAGE may be a predictor of mortality in CKD-G5D. We studied 123 CKD-G5D for 24 months. Of these patients, 56 were on hemodialysis (HD) and 67 on peritoneal dialysis (PD). Demographic, anthropometric, biochemical, and clinical data were recorded. sRAGE was quantified by enzyme-linked immunosorbent assay. sRAGE was a predictor of mortality at 2-year follow-up. Each increase of 100 pg/mL in sRAGE levels was associated with an approximately 7% increased risk of mortality. Furthermore, in the entire study group, as well as in PD and HD patient subgroups, sRAGE was positively correlated with brain natriuretic peptide (BNP) levels. Mortality rates as well as sRAGE levels in patients who died did not differ between PD and HD patients. In conclusion, the positive association observed with BNP levels suggests a role for sRAGE as a prognostic factor for mortality in CKD-G5D patients displaying an active process of cardiac remodeling.
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Enfermedades Cardiovasculares/metabolismo , Fallo Renal Crónico/metabolismo , Diálisis Peritoneal , Receptor para Productos Finales de Glicación Avanzada/metabolismo , Diálisis Renal , Anciano , Biomarcadores/metabolismo , Enfermedades Cardiovasculares/mortalidad , Enfermedades Cardiovasculares/terapia , Femenino , Humanos , Fallo Renal Crónico/mortalidad , Fallo Renal Crónico/terapia , Persona de Mediana Edad , Péptido Natriurético Encefálico/metabolismo , Estudios ProspectivosRESUMEN
PURPOSE: Soluble receptor for advanced glycation end products (sRAGE) is a decoy receptor which sequesters RAGE ligands and acts as a cytoprotective agent. To date, it is unclear whether the lower sRAGE levels observed in obesity are a marker of increased overall adiposity or reflect increases in particular fat depots. Therefore, we evaluated in healthy women the relationship among sRAGE and indicators of adiposity, including abdominal visceral (VAT) and epicardial visceral (EAT) adipose tissues, to explore the potential role of sRAGE as an earlier biomarker of cardiometabolic risk. METHODS: Plasma sRAGE levels were quantified by an enzyme-linked immunosorbent assay in 47 healthy women. Total fat mass (FM) and fat-free mass were estimated with bioimpedance analysis. Anthropometric measures and biochemical data were recorded. Subcutaneous adipose tissue, VAT and EAT volumes were measured by magnetic resonance imaging. RESULTS: Obese women had lower sRAGE levels compared to normal-weight women. sRAGE levels were also lower in women with a waist circumference (WC) larger than 80 cm. Correlation analyses indicated an inverse association of sRAGE with body mass index and FM. Concerning adipose tissue distribution, sRAGE inversely correlated with WC, EAT and VAT depots. In a multiple stepwise regression analysis, performed to emphasize the role of fat distribution, EAT volume was the only predictor of sRAGE. CONCLUSIONS: Lower sRAGE levels reflect accumulation of visceral fat mainly at the epicardial level and are present in advance of metabolic complications in adult women. sRAGE quantification might be an early marker of cardiometabolic risk.
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Composición Corporal , Distribución de la Grasa Corporal , Receptor para Productos Finales de Glicación Avanzada/sangre , Adiposidad , Adulto , Biomarcadores/sangre , Glucemia/metabolismo , Índice de Masa Corporal , Colesterol/sangre , Femenino , Humanos , Obesidad/sangre , Triglicéridos/sangre , Circunferencia de la Cintura , Salud de la MujerRESUMEN
Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.
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Factores de Crecimiento de Fibroblastos/metabolismo , Inflamación/metabolismo , Anciano , Biomarcadores/metabolismo , Proteína C-Reactiva/metabolismo , Estudios Transversales , Diabetes Mellitus/metabolismo , Femenino , Factor-23 de Crecimiento de Fibroblastos , Productos Finales de Glicación Avanzada/metabolismo , Humanos , Masculino , Persona de Mediana Edad , Receptor para Productos Finales de Glicación Avanzada/metabolismo , Albúmina Sérica/metabolismo , Albúmina Sérica GlicadaRESUMEN
An imbalance between degradation and reconstruction of the aortic wall is one of the leading causes of acute aortic dissection (AAD). Vitamin D seems an intriguing molecule to explore in the field of AAD since it improves endothelial function and protects smooth muscle cells from inflammation-induced remodeling, calcification, and loss of function, all events which are strongly related to the aging process. We quantified 25-hydroxy vitamin D, calcium, parathormone, bone alkaline phosphatase, and osteocalcin levels in 24 elderly AAD patients to identify a potential pathological implication of these molecules in AAD. Median 25-hydroxy vitamin D (10.75 ng/mL, 25th-75th percentiles: 6.86-19.23 ng/mL) and calcium levels (8.70 mg/dL, 25th-75th percentiles: 7.30-8.80 mg/dL) suggested hypovitaminosis D and a moderate hypocalcemia. Thirty-eight percent of AAD patients had severe (<10 ng/mL), 38% moderate (10-20 ng/mL), and 24% mild 25-hydroxy vitamin D deficiency (20-30 ng/mL). A significant inverse correlation was observed between 25OHD and osteocalcin levels. All the other molecules were unchanged. A condition of hypovitaminosis D associated to an increase in osteocalcin levels is present in AAD patients. The identification of these molecules as new factors involved in AAD may be helpful to identify individuals at high risk as well to study preventing strategies.
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Disección Aórtica/sangre , Osteocalcina/sangre , Deficiencia de Vitamina D/sangre , Vitamina D/análogos & derivados , Enfermedad Aguda , Anciano , Fosfatasa Alcalina/sangre , Calcio/sangre , Femenino , Humanos , Masculino , Persona de Mediana Edad , Hormona Paratiroidea/sangre , Proyectos Piloto , Vitamina D/sangreRESUMEN
BACKGROUND: Cardiotrophin-1 (CT-1), a cytokine produced by cardiomyocytes and non-cardiomyocytes in conditions of stress, can be used as a biomarker of left ventricular hypertrophy and dysfunction in hypertensive patients. Hypertension is one of the main adverse events in the third and last phase of Fabry's disease (FD). We measured CT-1 in order to examine its correlation with the vascular and cardiac alterations at different ages and assess its potential for use as a biomarker of hypertension in FD. FINDINGS: The level of CT-1 was clearly higher in hypertensive adults than in adult FD patients. FD patients show a small, non-significant decrease in plasma CT-1 with age, while in hypertensive patients CT-1 in plasma rises strongly and highly significantly with age. CONCLUSIONS: CT-1 can be considered a good biomarker of the progression of hypertension with age, but particular care is needed when following hypertension in FD patients, since CT-1 does not correlate the same way with this disease.
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BACKGROUND: Intense training can lead to a pathophysiological change in serum concentration of a variety of biomarkers. Traditional biomarkers of cardiac injury are very useful in monitoring CVD patients, but in healthy subjects or athletes they cannot be informative enough about the cardiovascular risk, because in these cases their serum levels do not increase over the pathological limit. Therefore novel cardiovascular biomarkers are required in order to allow a better monitoring of sport performance, prediction of overtraining and diagnosis of sport-related cardiac injuries. Growth differentiation factor-15 (GDF-15) is emerging as a powerful cardiovascular injury risk indicator. In this study we investigate the effect of intense physical training of on the circulating levels of GDF-15 in rugby professional players. METHODS: Serum GDF-15, Erythropoietin, IL-6, the cardiovascular parameter ST-2, NT-proBNP and routine hematological parameters were measured in a group of 30 rugby players before and after a session of intense training. RESULTS: While ST-2, IL-6 and hsCRP displayed no significant changes after intense training, NT-proBNP and GDF-15 showed a significant increase, even without reaching the pathological level. DISCUSSION: The measure of GDF-15 in professional rugby players could be a useful tool to monitoring their cardiovascular status during training and competition session in order to prevent the onset of collateral cardiovascular adverse event due to the intense training and, in the case of cardiac injury, it could possibly allow a very early diagnosis at the beginning of the pathogenic process.
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Biomarcadores/sangre , Sistema Cardiovascular/metabolismo , Ejercicio Físico , Factor 15 de Diferenciación de Crecimiento/sangre , Adulto , Humanos , MasculinoRESUMEN
Depressive disorders are highly prevalent among subjects suffering from chronic kidney disease (CKD). The aim of the present study is to evaluate clinical and biochemical factors associated with depressive disorders in a sample of older CKD patients, with a focus on advanced glycation end products (AGEs) and their soluble receptors (sRAGEs). A total of 115 older subjects affected by CKD (stages 3 to 5, not in dialysis) were selected for this study. These patients were divided into two groups according to the presence of depressive disorders defined by a score ≥ 10 on the 30-item Geriatric Depression Scale (GDS). The two groups were compared by independent sample t tests for continuous variables and χ2 tests for qualitative ones. Significant variables at univariate analyses were then inserted as predictors of a binary logistic regression model, with the presence or absence of depressive disorders as a dependent variable. The binary logistic regression model showed that patients with concomitant depressive disorders were more frequently of female gender (p < 0.01) and had lower MCP1 (p < 0.01) and AGE circulating levels (p < 0.01) than their counterparts. Depressive disorders in older CKD patients are more prevalent in women and seem to be inversely associated with systemic inflammation and circulating AGEs.
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BACKGROUND: Aging is considered an important independent risk factor for atherosclerosis. Down syndrome people (DS) display an accelerated aging process compared to healthy subjects, anyway they are relatively resistant to developing atherosclerosis. The mechanisms involved in such protective effect are not well known. Since heart-type fatty acid binding protein (H-FABP) is a protein involved in the transport of fatty acids and it has been recently correlated with the presence of atherosclerosis, we aimed to measure H-FABP level both in DS and in healthy subjects during aging to evaluate the association between this molecule, aging and atherosclerosis. FINDINGS: We quantified plasmatic H-FABP level in three groups of male DS and age-matched healthy subjects (children, age 2-14 years; adults, age 20-50 years; elderly, > 60 years) using a biochip array analyzer. We observed that aging is associated with increased H-FABP level in healthy subjects but not in DS which display both the same protein level in the different ages of life and have also lower level compared to their age-matched healthy subjects. CONCLUSION: Reduced H-FABP level during aging in DS may play a protective role against atherosclerosis. The potential involvement of H-FABP in the relationship between aging, atherosclerosis and development of coronary artery disease needs further investigations.