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  1. Article ; Online: p53 at the Intersection of Cardiac Fibroblast Proliferation and Activation: Answers and Questions.

    Ghigo, Alessandra / Ameri, Pietro

    Circulation research

    2023  Volume 133, Issue 3, Page(s) 288–290

    MeSH term(s) Tumor Suppressor Protein p53/genetics ; Heart ; Myocardium ; Fibroblasts ; Cell Proliferation
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2023-07-20
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cell-specific roles of p110β in myocardial ischaemia.

    Ghigo, Alessandra

    Cardiovascular research

    2019  Volume 115, Issue 8, Page(s) 1264–1265

    MeSH term(s) Cell Proliferation ; Class Ia Phosphatidylinositol 3-Kinase ; Humans ; Myocardial Ischemia ; Myocytes, Cardiac ; Ventricular Remodeling
    Chemical Substances Class Ia Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
    Language English
    Publishing date 2019-02-22
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvz051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: It Takes Two to Tango! Protein-Protein Interactions behind cAMP-Mediated CFTR Regulation.

    Murabito, Alessandra / Bhatt, Janki / Ghigo, Alessandra

    International journal of molecular sciences

    2023  Volume 24, Issue 13

    Abstract: Over the last fifteen years, with the approval of the first molecular treatments, a breakthrough era has begun for patients with cystic fibrosis (CF), the rare genetic disease caused by mutations in the gene encoding the cystic fibrosis transmembrane ... ...

    Abstract Over the last fifteen years, with the approval of the first molecular treatments, a breakthrough era has begun for patients with cystic fibrosis (CF), the rare genetic disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). These molecules, known as CFTR modulators, have led to unprecedented improvements in the lung function and quality of life of most CF patients. However, the efficacy of these drugs is still suboptimal, and the clinical response is highly variable even among individuals bearing the same mutation. Furthermore, not all patients carrying rare CFTR mutations are eligible for CFTR modulator therapies, indicating the need for alternative and/or add-on therapeutic approaches. Because the second messenger 3',5'-cyclic adenosine monophosphate (cAMP) represents the primary trigger for CFTR activation and a major regulator of different steps of the life cycle of the channel, there is growing interest in devising ways to fine-tune the cAMP signaling pathway for therapeutic purposes. This review article summarizes current knowledge regarding the role of cAMP signalosomes, i.e., multiprotein complexes bringing together key enzymes of the cAMP pathway, in the regulation of CFTR function, and discusses how modulating this signaling cascade could be leveraged for therapeutic intervention in CF.
    MeSH term(s) Humans ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Quality of Life ; Cystic Fibrosis/metabolism ; Cyclic AMP/metabolism ; Signal Transduction ; Mutation
    Chemical Substances Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Cyclic AMP (E0399OZS9N) ; CFTR protein, human
    Language English
    Publishing date 2023-06-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241310538
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Illuminating cAMP Dynamics at Ryanodine Receptors in Arrhythmias.

    Ghigo, Alessandra / Harvey, Robert D

    Circulation research

    2021  Volume 129, Issue 1, Page(s) 95–97

    MeSH term(s) Arrhythmias, Cardiac ; Humans ; Ryanodine Receptor Calcium Release Channel/genetics ; Sarcoplasmic Reticulum
    Chemical Substances Ryanodine Receptor Calcium Release Channel
    Language English
    Publishing date 2021-06-24
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.121.319449
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Editorial: Cardio-oncology and reverse cardio-oncology: the manifold interconnections between heart failure and cancer.

    Ghigo, Alessandra / Meijers, Wouter C / Rhee, June-Wha / Ameri, Pietro

    Frontiers in physiology

    2023  Volume 14, Page(s) 1205810

    Language English
    Publishing date 2023-05-09
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1205810
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: 'Circulating' RNA-based therapies in Cardio-Oncology.

    Tocchetti, Carlo G / Ghigo, Alessandra / Hirsch, Emilio

    European heart journal

    2022  Volume 43, Issue 42, Page(s) 4512–4514

    MeSH term(s) Humans ; Cardiotoxicity ; RNA, Circular ; Cell-Free Nucleic Acids ; Receptor, Insulin ; Neoplasms/genetics ; Neoplasms/therapy ; Doxorubicin
    Chemical Substances RNA, Circular ; Cell-Free Nucleic Acids ; Receptor, Insulin (EC 2.7.10.1) ; Doxorubicin (80168379AG)
    Language English
    Publishing date 2022-09-01
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehac407
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: cAMP/PKA signaling compartmentalization in cardiomyocytes: Lessons from FRET-based biosensors.

    Ghigo, Alessandra / Mika, Delphine

    Journal of molecular and cellular cardiology

    2019  Volume 131, Page(s) 112–121

    Abstract: 3',5'-cyclic adenosine monophosphate (cAMP) is a ubiquitous second messenger produced in response to the stimulation of G protein-coupled receptors (GPCRs). It regulates a plethora of pathophysiological processes in different organs, including the ... ...

    Abstract 3',5'-cyclic adenosine monophosphate (cAMP) is a ubiquitous second messenger produced in response to the stimulation of G protein-coupled receptors (GPCRs). It regulates a plethora of pathophysiological processes in different organs, including the cardiovascular system. It is now clear that cAMP is not uniformly distributed within cardiac myocytes but confined in specific subcellular compartments where it modulates key players of the excitation-contraction coupling as well as other processes including gene transcription, mitochondrial homeostasis and cell death. This review will cover the major cAMP microdomains in cardiac myocytes. We will describe recent work using pioneering tools developed for investigating the organization and the function of the major cAMP microdomains in cardiomyocytes, including the plasma membrane, the sarcoplasmic reticulum, the myofilaments, the nucleus and the mitochondria.
    MeSH term(s) Animals ; Biosensing Techniques/methods ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Excitation Contraction Coupling/physiology ; Fluorescence Resonance Energy Transfer/methods ; Humans ; Myocytes, Cardiac/metabolism ; Signal Transduction
    Chemical Substances Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2019-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2019.04.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 426: Show issues Location:
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  8. Article ; Online: The Interplay Between Autophagy and Senescence in Anthracycline Cardiotoxicity.

    Russo, Michele / Bono, Enrico / Ghigo, Alessandra

    Current heart failure reports

    2021  Volume 18, Issue 4, Page(s) 180–190

    Abstract: Purpose of review: Doxorubicin (DOXO) is a highly effective chemotherapeutic drug employed for the treatment of a wide spectrum of cancers, spanning from solid tumours to haematopoietic malignancies. However, its clinical use is hampered by severe and ... ...

    Abstract Purpose of review: Doxorubicin (DOXO) is a highly effective chemotherapeutic drug employed for the treatment of a wide spectrum of cancers, spanning from solid tumours to haematopoietic malignancies. However, its clinical use is hampered by severe and dose-dependent cardiac side effects that ultimately lead to heart failure (HF).
    Recent findings: Mitochondrial dysfunction and oxidative stress are well-established mechanisms of DOXO-induced cardiotoxicity, although recent evidence suggests that deregulation of other biological processes, like autophagy, could be involved. It is increasingly recognized that autophagy deregulation is intimately interconnected with the initiation of detrimental cellular responses, including autosis and senescence, raising the possibility of using autophagy modulators as well as senolytics and senomorphics for preventing DOXO cardiotoxicity. This review aims at providing an overview of the signalling pathways that are common to autophagy and senescence, with a special focus on how the relationship between these two processes is deregulated in response to cardiotoxic treatments. Finally, we will discuss the potential therapeutic utility of drugs modulating autophagy and/or senescence for counteracting DOXO cardiotoxicity.
    MeSH term(s) Anthracyclines/pharmacology ; Antibiotics, Antineoplastic/adverse effects ; Autophagy ; Cardiotoxicity ; Heart Failure/chemically induced ; Humans ; Myocytes, Cardiac
    Chemical Substances Anthracyclines ; Antibiotics, Antineoplastic
    Language English
    Publishing date 2021-06-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2151202-4
    ISSN 1546-9549 ; 1546-9530
    ISSN (online) 1546-9549
    ISSN 1546-9530
    DOI 10.1007/s11897-021-00519-w
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  9. Article ; Online: Cell signaling and regulation of CFTR expression in cystic fibrosis cells in the era of high efficiency modulator therapy.

    Ghigo, Alessandra / De Santi, Chiara / Hart, Merrill / Mitash, Nilay / Swiatecka-Urban, Agnieszka

    Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society

    2023  Volume 22 Suppl 1, Page(s) S12–S16

    Abstract: Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and protein kinase A (PKA)-regulated channel, expressed on the luminal surface of secretory and absorptive epithelial cells. CFTR has a complex, cell-specific regulatory network ... ...

    Abstract Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and protein kinase A (PKA)-regulated channel, expressed on the luminal surface of secretory and absorptive epithelial cells. CFTR has a complex, cell-specific regulatory network playing a major role in cAMP- and Ca
    MeSH term(s) Humans ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Electrolytes/metabolism ; Epithelial Sodium Channels/metabolism ; Signal Transduction
    Chemical Substances CFTR protein, human ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Electrolytes ; Epithelial Sodium Channels
    Language English
    Publishing date 2023-01-07
    Publishing country Netherlands
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2084724-5
    ISSN 1873-5010 ; 1569-1993
    ISSN (online) 1873-5010
    ISSN 1569-1993
    DOI 10.1016/j.jcf.2022.12.015
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  10. Article: Mechanisms of Anthracycline-Induced Cardiotoxicity: Is Mitochondrial Dysfunction the Answer?

    Murabito, Alessandra / Hirsch, Emilio / Ghigo, Alessandra

    Frontiers in cardiovascular medicine

    2020  Volume 7, Page(s) 35

    Abstract: Cardiac side effects are a major drawback of anticancer therapies, often requiring the use of low and less effective doses or even discontinuation of the drug. Among all the drugs known to cause severe cardiotoxicity are anthracyclines that, though being ...

    Abstract Cardiac side effects are a major drawback of anticancer therapies, often requiring the use of low and less effective doses or even discontinuation of the drug. Among all the drugs known to cause severe cardiotoxicity are anthracyclines that, though being the oldest chemotherapeutic drugs, are still a mainstay in the treatment of solid and hematological tumors. The recent expansion of the field of Cardio-Oncology, a branch of cardiology dealing with prevention or treatment of heart complications due to cancer treatment, has greatly improved our knowledge of the molecular mechanisms behind anthracycline-induced cardiotoxicity (AIC). Despite excessive generation of reactive oxygen species was originally believed to be the main cause of AIC, recent evidence points to the involvement of a plethora of different mechanisms that, interestingly, mainly converge on deregulation of mitochondrial function. In this review, we will describe how anthracyclines affect cardiac mitochondria and how these organelles contribute to AIC. Furthermore, we will discuss how drugs specifically targeting mitochondrial dysfunction and/or mitochondria-targeted drugs could be therapeutically exploited to treat AIC.
    Language English
    Publishing date 2020-03-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2020.00035
    Database MEDical Literature Analysis and Retrieval System OnLINE

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