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  1. Article ; Online: The Cardiovascular Phenotype in Fabry Disease

    Daniela Sorriento / Guido Iaccarino

    International Journal of Molecular Sciences, Vol 22, Iss 3, p

    New Findings in the Research Field

    2021  Volume 1331

    Abstract: Fabry disease (FD) is a lysosomal storage disorder, depending on defects in alpha-galactosidase A (GAL) activity. At the clinical level, FD shows a high phenotype variability. Among them, cardiovascular dysfunction is often recurrent or, in some cases, ... ...

    Abstract Fabry disease (FD) is a lysosomal storage disorder, depending on defects in alpha-galactosidase A (GAL) activity. At the clinical level, FD shows a high phenotype variability. Among them, cardiovascular dysfunction is often recurrent or, in some cases, is the sole symptom (cardiac variant) representing the leading cause of death in Fabry patients. The existing therapies, besides specific symptomatic treatments, are mainly based on the restoration of GAL activity. Indeed, mutations of the galactosidase alpha gene (GLA) cause a reduction or lack of GAL activity leading to globotriaosylceramide (Gb3) accumulation in several organs. However, several other mechanisms are involved in FD’s development and progression that could become useful targets for therapeutics. This review discusses FD’s cardiovascular phenotype and the last findings on molecular mechanisms that accelerate cardiac cell damage.
    Keywords fabry ; lysosomal disorder ; cardiovascular disease ; inflammation ; mitochondrial dysfunction ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Inflammation and Cardiovascular Diseases

    Daniela Sorriento / Guido Iaccarino

    International Journal of Molecular Sciences, Vol 20, Iss 16, p

    The Most Recent Findings

    2019  Volume 3879

    Abstract: The series of reactive biological events that we identify as inflammation has been investigated in recent years and unveiled as an important mechanism for regeneration. The study of the underlying complexity has been boosted by new technological ... ...

    Abstract The series of reactive biological events that we identify as inflammation has been investigated in recent years and unveiled as an important mechanism for regeneration. The study of the underlying complexity has been boosted by new technological innovation in research and allowed the identification of inflammatory responses as the basis of diseases that were considered degenerative rather than regenerative in nature. This is the case for cardiovascular diseases, from the organ damage that follows an acute event to the damage of target organs exposed to chronic risk factors. This editorial explores innovative aspects of inflammation in the setup of cardiovascular risk factors and diseases.
    Keywords inflammation ; NFκB ; cytokines ; inflammatory diseases ; heart failure ; cardiovascular risk ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2019-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Gene–environment interactions and vitamin D effects on cardiovascular risk

    Guido Iaccarino / Bruno Trimarco

    BMC Medicine, Vol 17, Iss 1, Pp 1-

    2019  Volume 2

    Keywords Vitamin D ; Genetics ; Environment ; Cardiovascular risk ; Supplementation ; Parathormone ; Medicine ; R
    Language English
    Publishing date 2019-08-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: NFkappaB is a Key Player in the Crosstalk between Inflammation and Cardiovascular Diseases

    Antonella Fiordelisi / Guido Iaccarino / Carmine Morisco / Enrico Coscioni / Daniela Sorriento

    International Journal of Molecular Sciences, Vol 20, Iss 7, p

    2019  Volume 1599

    Abstract: Inflammation is a key mechanism of cardiovascular diseases. It is an essential component of atherosclerosis and a significant risk factor for the development of cardiovascular events. In the crosstalk between inflammation and cardiovascular diseases, the ...

    Abstract Inflammation is a key mechanism of cardiovascular diseases. It is an essential component of atherosclerosis and a significant risk factor for the development of cardiovascular events. In the crosstalk between inflammation and cardiovascular diseases, the transcription factor NFκB seems to be a key player since it is involved in the development and progression of both inflammation and cardiac and vascular damage. In this review, we deal with the recent findings of the role of inflammation in cardiac diseases, focusing, in particular, on NFκB as a functional link. We describe strategies for the therapeutic targeting of NFκB as a potential strategy for the failing heart.
    Keywords inflammation ; cardiovascular diseases ; NFκB ; GRK ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2019-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Impaired mitochondrial calcium uptake caused by tacrolimus underlies beta-cell failure

    Angela Lombardi / Bruno Trimarco / Guido Iaccarino / Gaetano Santulli

    Cell Communication and Signaling, Vol 15, Iss 1, Pp 1-

    2017  Volume 7

    Abstract: Abstract Background One of the most common side effects of the immunosuppressive drug tacrolimus (FK506) is the increased risk of new-onset diabetes mellitus. However, the molecular mechanisms underlying this association have not been fully clarified. ... ...

    Abstract Abstract Background One of the most common side effects of the immunosuppressive drug tacrolimus (FK506) is the increased risk of new-onset diabetes mellitus. However, the molecular mechanisms underlying this association have not been fully clarified. Methods We studied the effects of the therapeutic dose of tacrolimus on mitochondrial fitness in beta-cells. Results We demonstrate that tacrolimus impairs glucose-stimulated insulin secretion (GSIS) in beta-cells through a previously unidentified mechanism. Indeed, tacrolimus causes a decrease in mitochondrial Ca2+ uptake, accompanied by altered mitochondrial respiration and reduced ATP production, eventually leading to impaired GSIS. Conclusion Our observations individuate a new fundamental mechanism responsible for the augmented incidence of diabetes following tacrolimus treatment. Indeed, this drug alters Ca2+ fluxes in mitochondria, thereby compromising metabolism-secretion coupling in beta-cells.
    Keywords Mitochondrial calcium ; ATP ; Diabetes ; Insulin release ; Immunosuppressive regimen ; Ca2+ leak ; Medicine ; R ; Cytology ; QH573-671
    Language English
    Publishing date 2017-11-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: The Metabolic Role of GRK2 in Insulin Resistance and Associated Conditions

    Daniela Sorriento / Maria Rosaria Rusciano / Valeria Visco / Antonella Fiordelisi / Federica Andrea Cerasuolo / Paolo Poggio / Michele Ciccarelli / Guido Iaccarino

    Cells, Vol 10, Iss 167, p

    2021  Volume 167

    Abstract: Insulin resistance (IRES) is a pathophysiological condition characterized by the reduced response to insulin of several tissues, including myocardial and skeletal muscle. IRES is associated with obesity, glucose intolerance, dyslipidemia, and ... ...

    Abstract Insulin resistance (IRES) is a pathophysiological condition characterized by the reduced response to insulin of several tissues, including myocardial and skeletal muscle. IRES is associated with obesity, glucose intolerance, dyslipidemia, and hypertension, evolves toward type 2 diabetes, and increases the risk of developing cardiovascular diseases. Several studies designed to explore the mechanisms involved in IRES allowed the identification of a multitude of potential molecular targets. Among the most promising, G Protein Coupled Receptor Kinase type 2 (GRK2) appears to be a suitable one given its functional implications in many cellular processes. In this review, we will discuss the metabolic role of GRK2 in those conditions that are characterized by insulin resistance (diabetes, hypertension, heart failure), and the potentiality of its inhibition as a therapeutic strategy to revert both insulin resistance and its associated phenotypes.
    Keywords GRK2 ; insulin resistance ; diabetes ; hypertension ; heart failure ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Renin-Angiotensin System Inhibition in Cardiovascular Patients at the Time of COVID19

    Guido Iaccarino , Claudio Borghi , Arrigo F G Cicero , Claudio Ferri , Pietro Minuz , Maria Lorenza Muiesan , Paolo Mulatero , Giuseppe Mulè , Giacomo Pucci , Massimo Salvetti , Carmine Savoia , Leonardo Alberto Sechi , Massimo Volpe , Guido Grassi

    Much Ado for Nothing? A Statement of Activity From the Directors of the Board and the Scientific Directors of the Italian Society of Hypertension

    2020  

    Abstract: Cardiovascular diseases, in particular hypertension, as well as the cardiovascular treatment with Renin-Angiotensin System inhibitors such as Angiotensin Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs), are claimed once again ... ...

    Abstract Cardiovascular diseases, in particular hypertension, as well as the cardiovascular treatment with Renin-Angiotensin System inhibitors such as Angiotensin Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs), are claimed once again as mechanisms of Severe Acute Respiratory Syndrome (SARS) during the COVID-19 outbreak due to Cov-2 epidemics. In vitro studies are available to support the eventual role of ACE inhibitors and ARBs in both the promotion and antagonism of the disease. The available literature, indeed, presents contrasting results, all concentrated in experimental models. Evidence in humans is lacking that those mechanisms are actually occurring in the present COVID-19 outbreak. Here we present the reasoned statement of the Italian Society of Hypertension to maintain ongoing antihypertensive treatments. Furthermore, the Italian Society of Hypertension presents its own initiative to investigate the issue using an online questionnaire to collect relevant data in human disease.
    Keywords COVID-19 ; cardiovascular diseases ; hypertension ; infection ; outcomes ; covid19
    Subject code 610
    Language English
    Publishing country it
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Diazoxide Improves Mitochondrial Connexin 43 Expression in a Mouse Model of Doxorubicin-Induced Cardiotoxicity

    Michela Pecoraro / Michele Ciccarelli / Antonella Fiordelisi / Guido Iaccarino / Aldo Pinto / Ada Popolo

    International Journal of Molecular Sciences, Vol 19, Iss 3, p

    2018  Volume 757

    Abstract: Doxorubicin (DOXO) administration induces alterations in Connexin 43 (Cx43) expression and localization, thus, inducing alterations in chemical and electrical signal transmission between cardiomyocytes and in intracellular calcium homeostasis even ... ...

    Abstract Doxorubicin (DOXO) administration induces alterations in Connexin 43 (Cx43) expression and localization, thus, inducing alterations in chemical and electrical signal transmission between cardiomyocytes and in intracellular calcium homeostasis even evident after a single administration. This study was designed to evaluate if Diazoxide (DZX), a specific opener of mitochondrial KATP channels widely used for its cardioprotective effects, can fight DOXO-induced cardiotoxicity in a short-time mouse model. DZX (20 mg/kg i.p.) was administered 30 min before DOXO (10 mg/kg i.p.) in C57BL/6j female mice for 1–3 or seven days once every other day. A recovery of cardiac parameters, evaluated by Echocardiography, were observed in DZX+DOXO co-treated mice. Western blot analysis performed on heart lysates showed an increase in sarco/endoplasmic reticulum Ca2+-ATPase (SERCAII) and a reduction in phospholamban (PLB) amounts in DZX+DOXO co-treated mice. A contemporary recovery of intracellular Ca2+-signal, detected spectrofluorometrically by means of FURA-2AM, was observed in these mice. Cx43 expression and localization, analyzed by Western blot and confirmed by immunofluorescence analysis, showed that DZX co-treatement increases Cx43 amount both on sarcoplasmic membrane and on mitochondria. In conclusion, our data demonstrate that, in a short-time mouse model of DOXO-induced cardiotoxicity, DZX exerts its cardioprotective effects also by enhancing the amount Cx43.
    Keywords diazoxide ; doxorubicin ; connexin 43 ; calcium homeostasis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2018-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Adrenergic Receptors and Metabolism

    MicheleCiccarelli / GaetanoSantulli / GuidoIaccarino

    Frontiers in Physiology, Vol

    Role in development of cardiovascular disease

    2013  Volume 4

    Abstract: Activation of the adrenergic system has a profound effects on metabolism. Increased circulating catecholamine and activation of the different adrenergic receptors deployed in the various organs produce important metabolic responses which include: 1) ... ...

    Abstract Activation of the adrenergic system has a profound effects on metabolism. Increased circulating catecholamine and activation of the different adrenergic receptors deployed in the various organs produce important metabolic responses which include: 1) increased lipolysis and elevated levels of fatty acids in plasma, 2) increased gluconeogenesis by the liver to provide substrate for the brain and 3) moderate inhibition of insulin release by the pancreas to conserve glucose and to shift fuel metabolism of muscle in the direction of fatty acid oxidation. These physiological responses, typical of the stress conditions, are demonstrated to be detrimental for the functioning of different organs like the cardiac muscle when they become chronic. Indeed, a common feature of many pathological conditions involving over-activation of the adrenergic system is the development of metabolic alterations which can include insulin resistance, altered glucose and lipid metabolism and mitochondrial dysfunction. These patterns are involved with a variably extent among the different pathologies , however they are in general strictly correlated to the level of activation of the adrenergic system. Here we will review the effects of the different adrenergic receptors subtypes on the metabolic variation observed in important disease like Heart Failure.
    Keywords Heart Failure ; Mitochondria ; GRKs ; cardiac metabolism ; Beta adrenergic system ; Physiology ; QP1-981 ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2013-10-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Experimental evidence and clinical implications of Warburg effect in the skeletal muscle of Fabry disease

    Jessica Gambardella / Antonella Fiordelisi / Federica Andrea Cerasuolo / Antonietta Buonaiuto / Roberta Avvisato / Alessandro Viti / Eduardo Sommella / Fabrizio Merciai / Emanuela Salviati / Pietro Campiglia / Valeria D’Argenio / Silvia Parisi / Antonio Bianco / Letizia Spinelli / Eugenio Di Vaia / Alberto Cuocolo / Antonio Pisani / Eleonora Riccio / Teodolinda Di Risi /
    Michele Ciccarelli / Gaetano Santulli / Daniela Sorriento / Guido Iaccarino

    iScience, Vol 26, Iss 3, Pp 106074- (2023)

    2023  

    Abstract: Summary: Skeletal muscle (SM) pain and fatigue are common in Fabry disease (FD). Here, we undertook the investigation of the energetic mechanisms related to FD-SM phenotype. A reduced tolerance to aerobic activity and lactate accumulation occurred in FD- ... ...

    Abstract Summary: Skeletal muscle (SM) pain and fatigue are common in Fabry disease (FD). Here, we undertook the investigation of the energetic mechanisms related to FD-SM phenotype. A reduced tolerance to aerobic activity and lactate accumulation occurred in FD-mice and patients. Accordingly, in murine FD-SM we detected an increase in fast/glycolytic fibers, mirrored by glycolysis upregulation. In FD-patients, we confirmed a high glycolytic rate and the underutilization of lipids as fuel. In the quest for a tentative mechanism, we found HIF-1 upregulated in FD-mice and patients. This finding goes with miR-17 upregulation that is responsible for metabolic remodeling and HIF-1 accumulation. Accordingly, miR-17 antagomir inhibited HIF-1 accumulation, reverting the metabolic-remodeling in FD-cells. Our findings unveil a Warburg effect in FD, an anaerobic-glycolytic switch under normoxia induced by miR-17-mediated HIF-1 upregulation. Exercise-intolerance, blood-lactate increase, and the underlying miR-17/HIF-1 pathway may become useful therapeutic targets and diagnostic/monitoring tools in FD.
    Keywords Cell biology ; Cellular physiology ; Health sciences ; Pathophysiology ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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