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  1. Article ; Online: Endothelin-1: Is it Time to "Biomark" the Cardiac-Tumor-Treatment Nexus in Breast Cancer?

    Valero-Muñoz, María / Sam, Flora

    JACC. CardioOncology

    2023  Volume 5, Issue 5, Page(s) 701–703

    Language English
    Publishing date 2023-10-17
    Publishing country United States
    Document type Editorial
    ISSN 2666-0873
    ISSN (online) 2666-0873
    DOI 10.1016/j.jaccao.2023.05.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A misdirected conundrum in translational HFpEF research.

    Valero-Muñoz, María / Sam, Flora

    Journal of molecular and cellular cardiology

    2022  Volume 168, Page(s) 1–2

    MeSH term(s) Heart Failure/genetics ; Humans ; Stroke Volume ; Translational Research, Biomedical ; Ventricular Function, Left
    Language English
    Publishing date 2022-04-08
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2022.04.003
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    Zs.A 426: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Reply to letter by Hou et al., Doxycycline ameliorates autophagy by inhibiting p38 MAPK in cardiac myocytes.

    Valero-Muñoz, María / Sam, Flora

    International journal of cardiology

    2021  Volume 331, Page(s) 212

    MeSH term(s) Autophagy ; Doxycycline/pharmacology ; Humans ; MAP Kinase Signaling System ; Myocytes, Cardiac/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2021-01-27
    Publishing country Netherlands
    Document type Letter ; Comment
    ZDB-ID 779519-1
    ISSN 1874-1754 ; 0167-5273
    ISSN (online) 1874-1754
    ISSN 0167-5273
    DOI 10.1016/j.ijcard.2021.01.016
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    Zs.A 1673: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Reply to letter by Ye et al., blocking lncRNA H19/miR-194-5p/SIRT1 axis in cardiac myocyte is responsible for doxycycline inhibiting autophagy.

    Valero-Muñoz, María / Sam, Flora

    International journal of cardiology

    2021  Volume 331, Page(s) 213

    MeSH term(s) Autophagy ; Doxycycline ; Humans ; MicroRNAs/genetics ; Myocytes, Cardiac ; RNA, Long Noncoding ; Sirtuin 1/genetics
    Chemical Substances MIRN194 microRNA, human ; MicroRNAs ; RNA, Long Noncoding ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2021-01-28
    Publishing country Netherlands
    Document type Letter ; Comment
    ZDB-ID 779519-1
    ISSN 1874-1754 ; 0167-5273
    ISSN (online) 1874-1754
    ISSN 0167-5273
    DOI 10.1016/j.ijcard.2021.01.021
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1673: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Reply: Diet-Induced Obesity HFpEF Murine Models.

    Valero-Muñoz, Maria / Sam, Flora

    JACC. Basic to translational science

    2018  Volume 3, Issue 1, Page(s) 158–159

    Language English
    Publishing date 2018-03-01
    Publishing country United States
    Document type Journal Article
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2018.01.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Heart Failure With Preserved Ejection Fraction: Heterogeneous Syndrome, Diverse Preclinical Models.

    Roh, Jason / Hill, Joseph A / Singh, Abhilasha / Valero-Muñoz, María / Sam, Flora

    Circulation research

    2022  Volume 130, Issue 12, Page(s) 1906–1925

    Abstract: Heart failure with preserved ejection fraction (HFpEF) represents one of the greatest challenges facing cardiovascular medicine today. Despite being the most common form of heart failure worldwide, there has been limited success in developing ... ...

    Abstract Heart failure with preserved ejection fraction (HFpEF) represents one of the greatest challenges facing cardiovascular medicine today. Despite being the most common form of heart failure worldwide, there has been limited success in developing therapeutics for this syndrome. This is largely due to our incomplete understanding of the biology driving its systemic pathophysiology and the heterogeneity of clinical phenotypes, which are increasingly being recognized as distinct HFpEF phenogroups. Development of efficacious therapeutics fundamentally relies on robust preclinical models that not only faithfully recapitulate key features of the clinical syndrome but also enable rigorous investigation of putative mechanisms of disease in the context of clinically relevant phenotypes. In this review, we propose a preclinical research strategy that is conceptually grounded in model diversification and aims to better align with our evolving understanding of the heterogeneity of clinical HFpEF. Although heterogeneity is often viewed as a major obstacle in preclinical HFpEF research, we challenge this notion and argue that embracing it may be the key to demystifying its pathobiology. Here, we first provide an overarching guideline for developing HFpEF models through a stepwise approach of comprehensive cardiac and extra-cardiac phenotyping. We then present an overview of currently available models, focused on the 3 leading phenogroups, which are primarily based on aging, cardiometabolic stress, and chronic hypertension. We discuss how well these models reflect their clinically relevant phenogroup and highlight some of the more recent mechanistic insights they are providing into the complex pathophysiology underlying HFpEF.
    MeSH term(s) Cardiovascular Agents ; Heart Failure/genetics ; Heart Failure/therapy ; Humans ; Stroke Volume/physiology
    Chemical Substances Cardiovascular Agents
    Language English
    Publishing date 2022-06-09
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.320257
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.70: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Ui IV Zs.60: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  7. Article ; Online: Skeletal muscle (dys)function in heart failure with preserved ejection fraction.

    Saw, Eng Leng / Ramachandran, Swetha / Valero-Muñoz, Maria / Sam, Flora

    Current opinion in cardiology

    2020  Volume 36, Issue 2, Page(s) 219–226

    Abstract: Purpose of review: Skeletal muscle dysfunction contributes to exercise intolerance, which manifests as dyspnea and fatiguability in patients with heart failure with preserved ejection fraction (HFpEF). This review aims to summarize the current ... ...

    Abstract Purpose of review: Skeletal muscle dysfunction contributes to exercise intolerance, which manifests as dyspnea and fatiguability in patients with heart failure with preserved ejection fraction (HFpEF). This review aims to summarize the current understanding of skeletal muscle dysfunction in HFpEF.
    Recent findings: Animal and human studies in HFpEF provide insights into the pathophysiological alterations in skeletal muscle structure and function with the identification of several molecular mechanisms. Exercise training and novel pharmacological therapies that target skeletal muscle are proposed as therapeutic interventions to treat HFpEF.
    Summary: There is evidence that skeletal muscle dysfunction plays a pathophysiological role in HFpEF. However, precise mechanistic insights are needed to understand the contribution of skeletal muscle dysfunction in HFpEF.
    MeSH term(s) Animals ; Exercise ; Exercise Tolerance ; Heart Failure/therapy ; Humans ; Muscle, Skeletal ; Stroke Volume
    Language English
    Publishing date 2020-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 645186-x
    ISSN 1531-7080 ; 0268-4705
    ISSN (online) 1531-7080
    ISSN 0268-4705
    DOI 10.1097/HCO.0000000000000824
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2556: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article: Proteomic and phosphoproteomic profiling in heart failure with preserved ejection fraction (HFpEF).

    Valero-Muñoz, María / Saw, Eng Leng / Hekman, Ryan M / Blum, Benjamin C / Hourani, Zaynab / Granzier, Henk / Emili, Andrew / Sam, Flora

    Frontiers in cardiovascular medicine

    2022  Volume 9, Page(s) 966968

    Abstract: Although the prevalence of heart failure with preserved ejection fraction (HFpEF) is increasing, evidence-based therapies for HFpEF remain limited, likely due to an incomplete understanding of this disease. This study sought to identify the cardiac- ... ...

    Abstract Although the prevalence of heart failure with preserved ejection fraction (HFpEF) is increasing, evidence-based therapies for HFpEF remain limited, likely due to an incomplete understanding of this disease. This study sought to identify the cardiac-specific features of protein and phosphoprotein changes in a murine model of HFpEF using mass spectrometry. HFpEF mice demonstrated moderate hypertension, left ventricle (LV) hypertrophy, lung congestion and diastolic dysfunction. Proteomics analysis of the LV tissue showed that 897 proteins were differentially expressed between HFpEF and Sham mice. We observed abundant changes in sarcomeric proteins, mitochondrial-related proteins, and NAD-dependent protein deacetylase sirtuin-3 (SIRT3). Upregulated pathways by GSEA analysis were related to immune modulation and muscle contraction, while downregulated pathways were predominantly related to mitochondrial metabolism. Western blot analysis validated SIRT3 downregulated cardiac expression in HFpEF vs. Sham (0.8 ± 0.0 vs. 1.0 ± 0.0;
    Language English
    Publishing date 2022-08-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2022.966968
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Skeletal muscle phenotypic switching in heart failure with preserved ejection fraction.

    Saw, Eng Leng / Werner, Louis Dominic / Zamani, Payman / Chirinos, Julio A / Valero-Muñoz, María / Sam, Flora

    Frontiers in cardiovascular medicine

    2022  Volume 9, Page(s) 1016452

    Abstract: Background: Skeletal muscle (SkM) phenotypic switching is associated with exercise intolerance in heart failure with preserved ejection fraction (HFpEF). Patients with HFpEF have decreased type-1 oxidative fibers and mitochondrial dysfunction, ... ...

    Abstract Background: Skeletal muscle (SkM) phenotypic switching is associated with exercise intolerance in heart failure with preserved ejection fraction (HFpEF). Patients with HFpEF have decreased type-1 oxidative fibers and mitochondrial dysfunction, indicative of impaired oxidative capacity. The
    Methods: HFpEF was induced in mice by uninephrectomy,
    Results: Histological analyses demonstrated a reduction in the abundance of oxidative fibers, type-2A fiber atrophy, decreased capillary density, and increased fibrotic area in the
    Conclusion: The HFpEF
    Language English
    Publishing date 2022-12-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2022.1016452
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Heart Failure With Preserved Ejection Fraction and Adipose Tissue: A Story of Two Tales.

    Oh, Albin / Okazaki, Ross / Sam, Flora / Valero-Muñoz, Maria

    Frontiers in cardiovascular medicine

    2019  Volume 6, Page(s) 110

    Abstract: Heart failure with preserved ejection fraction (HFpEF) is characterized by signs and symptoms of heart failure in the presence of a normal left ventricular ejection fraction. Although it accounts for up to 50% of all clinical presentations of heart ... ...

    Abstract Heart failure with preserved ejection fraction (HFpEF) is characterized by signs and symptoms of heart failure in the presence of a normal left ventricular ejection fraction. Although it accounts for up to 50% of all clinical presentations of heart failure, there are no evidence-based therapies for HFpEF to reduce morbidity and mortality. Additionally there is a lack of mechanistic understanding about the pathogenesis of HFpEF. HFpEF is associated with many comorbidities (such as obesity, hypertension, type 2 diabetes, atrial fibrillation, etc.) and is coupled with both cardiac and extra-cardiac abnormalities. Large outcome trials and registries reveal that being obese is a major risk factor for HFpEF. There is increasing focus on investigating the link between obesity and HFpEF, and the role that the adipose tissue and the heart, and the circulating milieu play in development and pathogenesis of HFpEF. This review discusses features of the obese-HFpEF phenotype and highlights proposed mechanisms implicated in the inter-tissue communication between adipose tissue and the heart in obesity-associated HFpEF.
    Language English
    Publishing date 2019-08-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2019.00110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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