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  1. Article ; Online: Editorial overview: Immune regulation and cancers.

    Giorgi, Carlotta / Kuchay, Shafi

    Current opinion in pharmacology

    2023  Volume 69, Page(s) 102360

    MeSH term(s) Humans ; Neoplasms/immunology
    Language English
    Publishing date 2023-03-02
    Publishing country England
    Document type Editorial
    ZDB-ID 2037057-X
    ISSN 1471-4973 ; 1471-4892
    ISSN (online) 1471-4973
    ISSN 1471-4892
    DOI 10.1016/j.coph.2023.102360
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5608: Show issues Location:
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  2. Article ; Online: The LRRC8C-STING-p53 axis in T cells: A Ca

    Missiroli, Sonia / Giorgi, Carlotta / Pinton, Paolo

    Cell calcium

    2022  Volume 105, Page(s) 102596

    Abstract: Up to now, no role has been associated with VRAC channels in T cells. In a recent paper published in Nature Immunology, LRRC8C has been described as an essential component of VRAC in T cells. These data raise the intriguing possibility that the LRRC8C- ... ...

    Abstract Up to now, no role has been associated with VRAC channels in T cells. In a recent paper published in Nature Immunology, LRRC8C has been described as an essential component of VRAC in T cells. These data raise the intriguing possibility that the LRRC8C-STING-p53 signaling axis may represent a new inhibitory pathway in T cells that controls their function and adaptive immunity.
    MeSH term(s) Membrane Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/metabolism ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Membrane Proteins ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2022-05-13
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2022.102596
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  3. Article ; Online: Measuring Mitochondrial Calcium Fluxes in Cardiomyocytes upon Mechanical Stretch-Induced Hypertrophy.

    Ramaccini, Daniela / Giorgi, Carlotta / Matter, Michelle L

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2475, Page(s) 215–222

    Abstract: Calcium Ca2+ regulation is a key component of numerous cellular functions. In cardiomyocytes, Ca2+ regulates excitation-contraction coupling and influences signaling cascades involved in cell metabolism and cell survival. Prolonged dysregulation of ... ...

    Abstract Calcium Ca2+ regulation is a key component of numerous cellular functions. In cardiomyocytes, Ca2+ regulates excitation-contraction coupling and influences signaling cascades involved in cell metabolism and cell survival. Prolonged dysregulation of mitochondrial Ca2+ leads to dysfunctional cardiomyocytes, apoptosis and ultimately heart failure. VEGF promotes cardiomyocyte contractility by increasing calcium transients to control the strength of the heartbeat. Here, we describe a method to measure mitochondrial Ca2+ fluxes in human ventricular cardiomocytes after inducing stretch-mediated hypertrophy in vitro.
    MeSH term(s) Calcium/metabolism ; Calcium Signaling ; Excitation Contraction Coupling ; Heart Ventricles ; Humans ; Hypertrophy/metabolism ; Myocytes, Cardiac/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-04-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2217-9_15
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  4. Article ; Online: Calcium Homeostasis in the Control of Mitophagy.

    Perrone, Mariasole / Patergnani, Simone / Di Mambro, Tommaso / Palumbo, Laura / Wieckowski, Mariusz R / Giorgi, Carlotta / Pinton, Paolo

    Antioxidants & redox signaling

    2023  Volume 38, Issue 7-9, Page(s) 581–598

    Abstract: Significance: ...

    Abstract Significance:
    MeSH term(s) Mitophagy ; Calcium/metabolism ; Mitochondria/metabolism ; Homeostasis ; Biological Transport ; Autophagy
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-03-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2022.0122
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    Zs.A 5488: Show issues Location:
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  5. Article ; Online: Molecular mechanisms and consequences of mitochondrial permeability transition.

    Bonora, Massimo / Giorgi, Carlotta / Pinton, Paolo

    Nature reviews. Molecular cell biology

    2021  Volume 23, Issue 4, Page(s) 266–285

    Abstract: Mitochondrial permeability transition (mPT) is a phenomenon that abruptly causes the flux of low molecular weight solutes (molecular weight up to 1,500) across the generally impermeable inner mitochondrial membrane. The mPT is mediated by the so-called ... ...

    Abstract Mitochondrial permeability transition (mPT) is a phenomenon that abruptly causes the flux of low molecular weight solutes (molecular weight up to 1,500) across the generally impermeable inner mitochondrial membrane. The mPT is mediated by the so-called mitochondrial permeability transition pore (mPTP), a supramolecular entity assembled at the interface of the inner and outer mitochondrial membranes. In contrast to mitochondrial outer membrane permeabilization, which mostly activates apoptosis, mPT can trigger different cellular responses, from the physiological regulation of mitophagy to the activation of apoptosis or necrosis. Although there are several molecular candidates for the mPTP, its molecular nature remains contentious. This lack of molecular data was a significant setback that prevented mechanistic insight into the mPTP, pharmacological targeting and the generation of informative animal models. In recent years, experimental evidence has highlighted mitochondrial F
    MeSH term(s) Animals ; Humans ; Adenosine Triphosphate ; Mammals ; Mitochondrial Membrane Transport Proteins/chemistry ; Mitochondrial Permeability Transition Pore ; Mitochondrial Transmembrane Permeability-Driven Necrosis
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore
    Language English
    Publishing date 2021-12-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2031313-5
    ISSN 1471-0080 ; 1471-0072
    ISSN (online) 1471-0080
    ISSN 1471-0072
    DOI 10.1038/s41580-021-00433-y
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    Zs.MG 26: Show issues

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  6. Article ; Online: Ca

    Marchi, Saverio / Giorgi, Carlotta / Galluzzi, Lorenzo / Pinton, Paolo

    Molecular cell

    2020  Volume 78, Issue 6, Page(s) 1055–1069

    Abstract: ... ...

    Abstract Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Humans ; Mitochondria/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Signal Transduction/physiology ; Transient Receptor Potential Channels/metabolism
    Chemical Substances Calcium Channels ; Transient Receptor Potential Channels ; mitochondrial calcium uniporter ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-06-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2020.04.017
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    Zs.A 5055: Show issues Location:
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  7. Article: The NLRP3 Inflammasome in Neurodegenerative Disorders: Insights from Epileptic Models.

    Palumbo, Laura / Carinci, Marianna / Guarino, Annunziata / Asth, Laila / Zucchini, Silvia / Missiroli, Sonia / Rimessi, Alessandro / Pinton, Paolo / Giorgi, Carlotta

    Biomedicines

    2023  Volume 11, Issue 10

    Abstract: Neuroinflammation represents a dynamic process of defense and protection against the harmful action of infectious agents or other detrimental stimuli in the central nervous system (CNS). However, the uncontrolled regulation of this physiological process ... ...

    Abstract Neuroinflammation represents a dynamic process of defense and protection against the harmful action of infectious agents or other detrimental stimuli in the central nervous system (CNS). However, the uncontrolled regulation of this physiological process is strongly associated with serious dysfunctional neuronal issues linked to the progression of CNS disorders. Moreover, it has been widely demonstrated that neuroinflammation is linked to epilepsy, one of the most prevalent and serious brain disorders worldwide. Indeed, NLRP3, one of the most well-studied inflammasomes, is involved in the generation of epileptic seizures, events that characterize this pathological condition. In this context, several pieces of evidence have shown that the NLRP3 inflammasome plays a central role in the pathophysiology of mesial temporal lobe epilepsy (mTLE). Based on an extensive review of the literature on the role of NLRP3-dependent inflammation in epilepsy, in this review we discuss our current understanding of the connection between NLRP3 inflammasome activation and progressive neurodegeneration in epilepsy. The goal of the review is to cover as many of the various known epilepsy models as possible, providing a broad overview of the current literature. Lastly, we also propose some of the present therapeutic strategies targeting NLRP3, aiming to provide potential insights for future studies.
    Language English
    Publishing date 2023-10-18
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11102825
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  8. Article ; Online: Comprehensive Analysis of Mitochondrial Dynamics Alterations in Heart Diseases.

    Morciano, Giampaolo / Boncompagni, Caterina / Ramaccini, Daniela / Pedriali, Gaia / Bouhamida, Esmaa / Tremoli, Elena / Giorgi, Carlotta / Pinton, Paolo

    International journal of molecular sciences

    2023  Volume 24, Issue 4

    Abstract: The most common alterations affecting mitochondria, and associated with cardiac pathological conditions, implicate a long list of defects. They include impairments of the mitochondrial electron transport chain activity, which is a crucial element for ... ...

    Abstract The most common alterations affecting mitochondria, and associated with cardiac pathological conditions, implicate a long list of defects. They include impairments of the mitochondrial electron transport chain activity, which is a crucial element for energy formation, and that determines the depletion of ATP generation and supply to metabolic switches, enhanced ROS generation, inflammation, as well as the dysregulation of the intracellular calcium homeostasis. All these signatures significantly concur in the impairment of cardiac electrical characteristics, loss of myocyte contractility and cardiomyocyte damage found in cardiac diseases. Mitochondrial dynamics, one of the quality control mechanisms at the basis of mitochondrial fitness, also result in being dysregulated, but the use of this knowledge for translational and therapeutic purposes is still in its infancy. In this review we tried to understand why this is, by summarizing methods, current opinions and molecular details underlying mitochondrial dynamics in cardiac diseases.
    MeSH term(s) Humans ; Mitochondrial Dynamics/physiology ; Heart Diseases/metabolism ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; Mitochondria, Heart/metabolism
    Language English
    Publishing date 2023-02-08
    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/ijms24043414
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  9. Article: SARS-CoV-2 Infection Prompts IL-1β-Mediated Inflammation and Reduces IFN-λ Expression in Human Lung Tissue.

    Vezzani, Bianca / Neri, Margherita / D'Errico, Stefano / Papi, Alberto / Contoli, Marco / Giorgi, Carlotta

    Pathogens (Basel, Switzerland)

    2022  Volume 11, Issue 11

    Abstract: Two years after its spreading, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still responsible for more than 2000 deaths per day worldwide, despite vaccines and monoclonal antibody countermeasures. Therefore, there is a need to ... ...

    Abstract Two years after its spreading, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still responsible for more than 2000 deaths per day worldwide, despite vaccines and monoclonal antibody countermeasures. Therefore, there is a need to understand the immune-inflammatory pathways that prompt the manifestation of the disease to identify a novel potential target for pharmacological intervention. In this context, the characterization of the main players in the SARS-CoV-2-induced cytokine storm is mandatory. To date, the most characterized have been IL-6 and the class I and II interferons, while less is known about the proinflammatory cytokine IL-1β and class III interferons. Here, we report a preliminary study aimed at the characterization of the lung inflammatory context in COVID-19 patients, with a special focus on IFN-λ and IL-1β. By investigating IFN and inflammatory cytokine patterns by IHC in 10 deceased patients due to COVID-19 infection, compared to 10 control subjects, we reveal that while IFN-β production was increased in COVID-19 patients, IFN-λ was almost abolished. At the same time, the levels of IL-1β were dramatically improved, while IL-6 lung levels seem to be unaffected by the infection. Our findings highlight a central role of IL-1β in prompting lung inflammation after SARS-CoV-2 infection. Together, we show that IFN-λ is negatively affected by viral infection, supporting the idea that IFN-λ administration together with the pharmaceutical blockage of IL-1β represents a promising approach to revert the COVID-19-induced cytokine storm.
    Language English
    Publishing date 2022-11-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens11111390
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  10. Article ; Online: The inhibition of MDM2 slows cell proliferation and activates apoptosis in ADPKD cell lines.

    Patergnani, Simone / Giattino, Antonino / Bianchi, Nicoletta / Giorgi, Carlotta / Pinton, Paolo / Aguiari, Gianluca

    Biology of the cell

    2022  

    Abstract: Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is characterised by progressive cysts formation and renal enlargement that in most of cases leads to end stage of renal disease (ESRD). This pathology is caused by mutations of either ... ...

    Abstract Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is characterised by progressive cysts formation and renal enlargement that in most of cases leads to end stage of renal disease (ESRD). This pathology is caused by mutations of either PKD1 or PKD2 genes that encode for polycystin-1 (PC1) and polycystin-2 (PC2), respectively. These proteins function as receptor-channel complex able to regulate calcium homeostasis. PKD1/2 loss of function impairs different signalling pathways including cAMP and mTOR that are considered therapeutic targets for this disease. In fact, Tolvaptan, a vasopressin-2 antagonist that reduces cAMP levels, is the only drug approved for ADPKD treatment. Nevertheless, some ADPKD patients developed side effects in response to Tolvaptan including liver damage. Conversely, mTOR inhibitors that induced disease regression in ADPKD animal models failed the clinical trials.
    Results: Here, we show that the inhibition of mTOR causes the activation of autophagy in ADPKD cells that could reduce therapy effectiveness by drug degradation through the autophagic vesicles. Consistently, the combined treatment with rapamycin and chloroquine, an autophagy inhibitor, potentiates the decrease of cell proliferation induced by rapamycin. To overcome the dangerous activation of autophagy by mTOR inhibition, we targeted MDM2 (a downstream effector of mTOR signalling) that is involved in TP53 degradation by using RG7112, a small-molecule MDM2 inhibitor used for the treatment of haematologic malignancies. The inhibition of MDM2 by RG7112 prevents TP53 degradation and increases p21 expression leading to the decrease of cell proliferation and the activation of apoptosis.
    Conclusion: The targeting of MDM2 by RG7112 might represent a new therapeutic option for the treatment of ADPKD.
    Language English
    Publishing date 2022-09-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 245745-3
    ISSN 1768-322X ; 0399-0311 ; 0248-4900
    ISSN (online) 1768-322X
    ISSN 0399-0311 ; 0248-4900
    DOI 10.1111/boc.202200037
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