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  • 1
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    Trehalose, a natural disaccharide, reduces stroke occurrence in the stroke-prone spontaneously hypertensive rat
    Elsevier BV ; 2021
    In:  Pharmacological Research Vol. 173 ( 2021-11), p. 105875-
    Details
    In: Pharmacological Research, Elsevier BV, Vol. 173 ( 2021-11), p. 105875-
    Type of Medium: Online Resource
    ISSN: 1043-6618
    URL: Article
    DOI: 10.1016/j.phrs.2021.105875
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1471456-5
    SSG: 15,3
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  • 2
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    A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling
    Hindawi Limited ; 2017
    In:  Oxidative Medicine and Cellular Longevity Vol. 2017 ( 2017), p. 1-16
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2017 ( 2017), p. 1-16
    Abstract: Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2017/3920195
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2017
    detail.hit.zdb_id: 2455981-7
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  • 3
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    Protective Effects of Oroxylin A against Doxorubicin-Induced Cardiotoxicity via the Activation of Sirt1 in Mice
    Hindawi Limited ; 2021
    In:  Oxidative Medicine and Cellular Longevity Vol. 2021 ( 2021-1-19), p. 1-11
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-1-19), p. 1-11
    Abstract: Doxorubicin- (DOX-) related cardiac injury impairs the life quality of patients with cancer. This largely limited the clinical use of DOX. It is of great significance to find a novel strategy to reduce DOX-related cardiac injury. Oroxylin A (OA) has been identified to exert beneficial effects against inflammatory diseases and cancers. Here, we investigated whether OA could attenuate DOX-induced acute cardiotoxicity in mice. A single dose of DOX was used to induce acute cardiac injury in mice. To explore the protective effects, OA was administered to mice for ten days beginning from five days before DOX injection. The data in our study indicated that OA inhibited DOX-induced heart weight loss, reduction in cardiac function, and the elevation in myocardial injury markers. DOX injection resulted in increased oxidative damage, inflammation accumulation, and myocardial apoptosis in vivo and in vitro, and these pathological alterations were alleviated by treatment of OA. OA activated the sirtuin 1 (Sirt1) signaling pathway via the cAMP/protein kinase A, and its protective effects were blocked by Sirt1 deficiency. OA treatment did not affect the tumor-killing action of DOX in tumor-bearing mice. In conclusion, OA protected against DOX-related acute cardiac injury via the regulation of Sirt1.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2021/6610543
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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  • 4
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    Deregulation of Notch1 pathway and circulating endothelial progenitor cell (EPC) number in patients with bicuspid aortic valve with and without ascending aorta aneurysm
    Springer Science and Business Media LLC ; 2018
    In:  Scientific Reports Vol. 8, No. 1 ( 2018-09-14)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-09-14)
    Abstract: Bicuspid aortic valve (BAV) is frequently associated with the development of ascending aortic aneurysm, even if the underlying mechanisms remain to be clarified. Here, we investigated if a deregulation of Notch1 signaling pathway and endothelial progenitor cells (EPCs) number is associated with BAV disease and an early ascending aortic aneurysm (AAA) onset. For this purpose, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mean age: 69.1 ± 12.8 years) and AAA complicated or not, were included. Interestingly, patients with AAA showed a significant increase in circulating Notch1 levels and EPC number than subjects without AAA. However, circulating Notch1 levels and EPC number were significantly lower in BAV subjects than TAV patients either in the presence or absence of AAA. Finally, Notch pathway was activated to a greater extent in aortic aneurysmatic portions with respect to healthy aortic fragments in both BAV and TAV patients. However, the expression of genes encoding components and ligands of Notch pathway in aortic tissues was significantly lower in BAV than TAV subjects. Our study demonstrates that BAV subjects are characterized by a significant decrease in both tissue and circulating levels of Notch pathway, and in blood EPC number than TAV patients, either in presence or absence of AAA disease.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-018-32170-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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  • 5
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    275 MST1 MEDIATES DOXORUBICIN-INDUCED CARDIOMYOPATHY BY SIRT3 DOWNREGULATION
    Oxford University Press (OUP) ; 2022
    In:  European Heart Journal Supplements Vol. 24, No. Supplement_K ( 2022-12-15)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 24, No. Supplement_K ( 2022-12-15)
    Abstract: Heart failure is a major side effect of doxorubicin (DOX) treatment in patients with cancer. However, the mechanisms underlying the development of DOX-induced cardiomyopathy (DCM) need to be addressed. Here, we demonstrate that the serine/threonine kinase MST1, a major Hippo pathway component, contributes to the development of DOX-induced myocardial injury. Hypothesis The inhibition of MST1 protects from DCM by preserving SIRT3 expression Methods C57BL/6J WT mice and mice with cardiomyocyte-specific dominant-negative MST1 (kinase-dead) overexpression received 3 weekly injections of DOX, reaching a final cumulative dose of 18 mg/kg. Echocardiographic, histological and biochemical analyses were performed 6 weeks after the first administration of DOX. Results MST1 signaling was significantly activated in cardiomyocytes in response to DOX treatment in vitro and in vivo. Wild-type (WT) mice treated with DOX had reduced fractional shortening (46,1±1,77 vs. 31,1±1,07, n=7-11) and mitochondrial abnormalities (3,7±0,93 vs. 10,2±1,5, n=12 microscopic fields from 3 independent samples). However, systolic dysfunction was abolished in mice with cardiomyocyte-specific overexpression of dominant-negative MST1 (DN-MST1) (31,1±1,07 vs. 46,3±1,13, n=11) or treated with the MST1 inhibitor ‘XMU-MP-1’ (37,5±1,8 vs. 46,6±1,87, n=8), indicating that MST1 inhibition attenuates DOX-induced cardiac dysfunction. Also, DOX treatment led to a significant downregulation of cardiac levels of SIRT3 (1±0,12 vs. 0,6±0,11, n=4), a deacetylase involved in mitochondrial protection, in WT mice, which was rescued by MST1 inhibition (0,6±0,11 vs. 1,3±0,04, n=4). Pharmacological inhibition of SIRT3 blunted the protective effects of MST1 inhibition (44,5±1,55 vs. 32,5±2,33, n=4), indicating that SIRT3 downregulation mediates the cytotoxic effects of MST1 activation in response to DOX treatment. Finally, we found a significant upregulation of MST1 levels in human myocardial tissue of cancer patients treated with DOX (1,5±0,23 vs. 2,4±0,12, N=81-123 cells from 3 different patients). Conclusion MST1 contributes to DOX-induced cardiomyopathy by promoting mitochondrial damage through SIRT3 downregulation in cardiomyocytes.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartjsupp/suac121.138
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2141255-8
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  • 6
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    Cerebrovascular Complications and Infective Endocarditis: Impact of Available Evidence on Clinical Outcome
    Hindawi Limited ; 2018
    In:  BioMed Research International Vol. 2018 ( 2018-12-30), p. 1-6
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2018 ( 2018-12-30), p. 1-6
    Abstract: Background . Infective endocarditis (IE) is a life-threatening disease. Its epidemiological profile has substantially changed in recent years although 1-year mortality is still high. Despite advances in medical therapy and surgical technique, there is still uncertainty on the best management and on the timing of surgical intervention. The objective of this review is to produce further insight into the short- and long-term outcomes of patients with IE, with a focus on those presenting cerebrovascular complications.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2018/4109358
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
    detail.hit.zdb_id: 2698540-8
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  • 7
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    Abstract 14894: Mst1 Mediates Doxorubicin-Induced Cardiomyopathy by Sirt3 Downregulation
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: INTRODUCTION: Heart failure is a major side effect of doxorubicin (DOX) treatment in patients with cancer. However, the mechanisms underlying the development of DOX-induced cardiomyopathy (DCM) need to be addressed. Here, we demonstrate that the serine/threonine kinase MST1, a major component of the Hippo pathway, contributes to the development of DOX-induced myocardial injury. HYPOTHESIS: The inhibition of MST1 protects from DCM by preserving SIRT3 expression METHODS: C57BL/6J WT mice and mice with cardiomyocyte-specific dominant-negative MST1 (kinase-dead, DN-MST1) overexpression received 3 weekly injections of DOX, reaching a final cumulative dose of 18 mg/kg. Echocardiographic, histological and biochemical analyses were performed 6 weeks after the first administration of DOX. RESULTS: MST1 signaling was significantly activated in cardiomyocytes in response to DOX treatment in vitro and in vivo. Wild-type (WT) mice treated with DOX had reduced fractional shortening (46,1±1,8 vs. 31,1±1,1, n=7-11, p 〈 0.0001) and TEM mitochondrial abnormalities (3,7±0,9 vs. 10,2±1,5, n=12, p 〈 0.0001). However, systolic dysfunction was abolished in mice with CM-specific overexpression of DN-MST1 (31,1±1,1 vs. 46,3±1,1, n=11, p 〉 0.0001) or treated with the MST1 inhibitor ‘XMU-MP-1’ (37,5±1,8 vs. 46,6±1,9, n=8, p 〈 0.01), indicating that MST1 inhibition attenuates DOX-induced cardiac dysfunction. DOX treatment also led to a significant downregulation of cardiac levels of SIRT3 (1±0,1 vs. 0,6±0,1, p 〈 0.05), a deacetylase involved in mitochondrial protection, in WT mice, which was rescued by MST1 inhibition (0,6±0,1 vs. 1,3±0,04, p 〈 0.001). Pharmacological inhibition of SIRT3 blunted the protective effects of MST1 inhibition (44,5±1,6 vs. 32,5±2,3, n=4, p 〈 0.01), indicating that SIRT3 downregulation mediates the cytotoxic effects of MST1 activation in response to DOX treatment. Finally, we found a significant upregulation of MST1 levels in human myocardial tissue of cancer patients treated with DOX (1,5±0,23 vs. 2,4±0,12, N=81-123 cells from 3 different patients, p 〈 0.001). CONCLUSION: MST1 contributes to DOX-induced cardiomyopathy by promoting mitochondrial damage through SIRT3 downregulation in cardiomyocytes.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.14894
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 8
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    Mitochondria and Doxorubicin-Induced Cardiomyopathy: A Complex Interplay
    MDPI AG ; 2022
    In:  Cells Vol. 11, No. 13 ( 2022-06-22), p. 2000-
    Details
    In: Cells, MDPI AG, Vol. 11, No. 13 ( 2022-06-22), p. 2000-
    Abstract: Cardiotoxicity has emerged as a major side effect of doxorubicin (DOX) treatment, affecting nearly 30% of patients within 5 years after chemotherapy. Heart failure is the first non-cancer cause of death in DOX-treated patients. Although many different molecular mechanisms explaining the cardiac derangements induced by DOX were identified in past decades, the translation to clinical practice has remained elusive to date. This review examines the current understanding of DOX-induced cardiomyopathy (DCM) with a focus on mitochondria, which were increasingly proven to be crucial determinants of DOX-induced cytotoxicity. We discuss DCM pathophysiology and epidemiology and DOX-induced detrimental effects on mitochondrial function, dynamics, biogenesis, and autophagy. Lastly, we review the current perspectives to contrast the development of DCM, which is still a relatively diffused, invalidating, and life-threatening condition for cancer survivors.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells11132000
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2661518-6
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  • 9
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    C2238 ANP gene variant promotes increased platelet aggregation through the activation of Nox2 and the reduction of cAMP
    Springer Science and Business Media LLC ; 2017
    In:  Scientific Reports Vol. 7, No. 1 ( 2017-06-19)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-06-19)
    Abstract: Subjects carrying the C2238 variant of the atrial natriuretic peptide (ANP) gene have a higher occurrence of stroke and acute coronary syndrome, suggesting an increased predisposition to acute thrombotic events in these subjects. We evaluated for the first time the direct effects of mutant ANP (C2238/αANP) on platelet activation in vitro and in human subjects. In vitro , platelets were incubated with no peptide, with T2238/αANP (WT) or with C2238/αANP at different concentrations. C2238/αANP (10 −10 M) induced higher collagen-induced platelet aggregation with respect to both control without ANP and T2238/αANP. This effect was even stronger at a higher concentration (10 −6 M). Mechanistically, C2238/αANP significantly lowered platelet cAMP levels, increased ROS production and activated Nox2, with respect to both control and T2238/αANP. Forskolin, a cAMP activator, and sNOX2-tat, a Nox2 inhibitor, significantly reduced the pro-aggregant effects of C2238/αANP. In vivo , we found that platelet aggregation resulted to be higher in patients with atrial fibrillation carrying the C2238 ANP gene variant with respect to non-carriers. In conclusions, C2238/αANP promotes platelet aggregation through the activation of Nox2 and the reduction of cAMP.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-017-03679-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2615211-3
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  • 10
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    Abstract 15487: Boosting Autophagy for the Reduction of Diabetes-Induced Endothelial Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Introduction: Diabetes is one of the main cause of endothelial dysfunction. The molecular mechanisms underlying the effects of hyperglycaemia in endothelial cells still need to be clarified. Autophagy, a stress-responsive and self-renewal mechanism exerts beneficial effects in the cardiovascular system. However, its role in diabetes-induced endothelial dysfunction is unknown. Hypothesis: Endothelial autophagy is impaired in the presence of diabetes and restoration of autophagy may reduce diabetes-induced endothelial damage. Methods: The effects of hyperglycaemia (HG, 30 mM for 6 and 24 hours) on autophagy, mitophagy and endothelial function were evaluated in vitro in human umbilical endothelial cells (HUVEC). Vascular reactivity experiments were performed in mesenteric arteries from wild-type mice (WT) treated with HG and in human saphenous veins from patients with peripheral artery diseases. Autophagy reactivation was carried out through ATG7 overexpression (ATG7ov) or through spermidine (SP) (100 nM), a natural activator of autophagy and inhibitor of p300. Results: HG reduces autophagy (0.6 fold p 〈 0.05) and mitophagy (1.5 fold p 〈 0.001) in endothelial cells. HG also inhibits stress-induced autophagy in cells undergoing hypoxia (0.6 fold p 〈 0.05). ATG7ov rescues apoptosis (0.52 fold p 〈 0.05) and angiogenesis (2.3 fold p 〈 0.05) in HUVEC exposed to HG treatment. We found increased expression of the histone acetyltransferase p300 (2.27 fold p 〈 0.05), a known inhibitor of autophagy. Knockout mice of autophagy (Beclin 1 +/-) show a reduction in endothelial-dependent vasorelaxation compared to WT mice in response to HG (-19.16 % +-4.97 SEM vs -48.39 % +-2.18 SEM p 〈 0.001). Autophagy reactivation through ATG7ov or spermidine rescues endothelial-dependent relaxation in WT mice treated with HG (ATG7ov -62.48 % +-5.16 SEM; SP -63.01 +-3.22 SEM; HG -40.67 % +-3.82 p 〈 0.001). Finally, we demonstrated that SP improves vascular function in human veins (-37.6 % +-12.76 SEM vs -12.52 % +-5.6 SEM p 〈 0.001). Conclusions: The impairment of autophagy in response to diabetes contributes to endothelial dysfunction. Boosting autophagy with natural activators of autophagy may be a suitable intervention to reduce vascular damage in the presence of metabolic stress.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.15487
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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