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  1. Article: Editorial: Targeting the Wnt/β-catenin signaling pathway in cancer.

    Patergnani, Simone / Buchsbaum, Donald J / Piazza, Gary A

    Frontiers in oncology

    2022  Volume 12, Page(s) 1022174

    Language English
    Publishing date 2022-09-13
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.1022174
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Editorial: Organelles Relationships and Interactions: A Cancer Perspective.

    Patergnani, Simone / Marchi, Saverio / Delprat, Benjamin / Wieckowski, Mariusz R

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 678307

    Language English
    Publishing date 2021-04-08
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.678307
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5488: 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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  4. Article ; Online: Osteosarcoma cell death induced by innovative scaffolds doped with chemotherapeutics.

    Lanzillotti, Carmen / Iaquinta, Maria Rosa / De Pace, Raffaella / Mosaico, Maria / Patergnani, Simone / Giorgi, Carlotta / Tavoni, Marta / Dapporto, Massimiliano / Sprio, Simone / Tampieri, Anna / Montesi, Monica / Martini, Fernanda / Mazzoni, Elisa

    Journal of cellular physiology

    2024  

    Abstract: Osteosarcoma (OS) cancer treatments include systemic chemotherapy and surgical resection. In the last years, novel treatment approaches have been proposed, which employ a drug-delivery system to prevent offside effects and improves treatment efficacy. ... ...

    Abstract Osteosarcoma (OS) cancer treatments include systemic chemotherapy and surgical resection. In the last years, novel treatment approaches have been proposed, which employ a drug-delivery system to prevent offside effects and improves treatment efficacy. Locally delivering anticancer compounds improves on high local concentrations with more efficient tumour-killing effect, reduced drugs resistance and confined systemic effects. Here, the synthesis of injectable strontium-doped calcium phosphate (SrCPC) scaffold was proposed as drug delivery system to combine bone tissue regeneration and anticancer treatment by controlled release of methotrexate (MTX) and doxorubicin (DOX), coded as SrCPC-MTX and SrCPC-DOX, respectively. The drug-loaded cements were tested in an in vitro model of human OS cell line SAOS-2, engineered OS cell line (SAOS-2-eGFP) and U2-OS. The ability of doped scaffolds to induce OS cell death and apoptosis was assessed analysing cell proliferation and Caspase-3/7 activities, respectively. To determine if OS cells grown on doped-scaffolds change their migratory ability and invasiveness, a wound-healing assay was performed. In addition, the osteogenic potential of SrCPC material was evaluated using human adipose derived-mesenchymal stem cells. Osteogenic markers such as (i) the mineral matrix deposition was analysed by alizarin red staining; (ii) the osteocalcin (OCN) protein expression was investigated by enzyme-linked immunosorbent assay test, and (iii) the osteogenic process was studied by real-time polymerase chain reaction array. The delivery system induced cell-killing cytotoxic effects and apoptosis in OS cell lines up to Day 7. SrCPC demonstrates a good cytocompatibility and it induced upregulation of osteogenic genes involved in the skeletal development pathway, together with OCN protein expression and mineral matrix deposition. The proposed approach, based on the local, sustained release of anticancer drugs from nanostructured biomimetic drug-loaded cements is promising for future therapies aiming to combine bone regeneration and anticancer local therapy.
    Language English
    Publishing date 2024-04-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.31256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.212: Show issues Location:
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  5. Article ; Online: The Wolfram-like variant WFS1

    Patergnani, Simone / Bataillard, Méghane S / Danese, Alberto / Alves, Stacy / Cazevieille, Chantal / Valéro, René / Tranebjærg, Lisbeth / Maurice, Tangui / Pinton, Paolo / Delprat, Benjamin / Richard, Elodie M

    Autophagy

    2024  , Page(s) 1–12

    Abstract: Dominant variants ... ...

    Abstract Dominant variants in
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2024.2341588
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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  6. Article: Update on Calcium Signaling in Cystic Fibrosis Lung Disease.

    Rimessi, Alessandro / Vitto, Veronica A M / Patergnani, Simone / Pinton, Paolo

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 581645

    Abstract: Cystic fibrosis (CF) is an autosomal recessive disorder characterized by mutations in the cystic fibrosis transmembrane conductance regulator gene, which causes multifunctional defects that preferentially affect the airways. Abnormal viscosity of mucus ... ...

    Abstract Cystic fibrosis (CF) is an autosomal recessive disorder characterized by mutations in the cystic fibrosis transmembrane conductance regulator gene, which causes multifunctional defects that preferentially affect the airways. Abnormal viscosity of mucus secretions, persistent pathogen infections, hyperinflammation, and lung tissue damage compose the classical pathological manifestation referred to as CF lung disease. Among the multifunctional defects associated with defective CFTR, increasing evidence supports the relevant role of perturbed calcium (Ca
    Language English
    Publishing date 2021-03-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.581645
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Mitochondrial Oxidative Stress and "Mito-Inflammation": Actors in the Diseases.

    Patergnani, Simone / Bouhamida, Esmaa / Leo, Sara / Pinton, Paolo / Rimessi, Alessandro

    Biomedicines

    2021  Volume 9, Issue 2

    Abstract: A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate ... ...

    Abstract A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.
    Language English
    Publishing date 2021-02-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines9020216
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: The "mitochondrial stress responses": the "Dr. Jekyll and Mr. Hyde" of neuronal disorders.

    Patergnani, Simone / Morciano, Giampaolo / Carinci, Marianna / Leo, Sara / Pinton, Paolo / Rimessi, Alessandro

    Neural regeneration research

    2022  Volume 17, Issue 12, Page(s) 2563–2575

    Abstract: Neuronal disorders are associated with a profound loss of mitochondrial functions caused by various stress conditions, such as oxidative and metabolic stress, protein folding or import defects, and mitochondrial DNA alteration. Cells engage in different ... ...

    Abstract Neuronal disorders are associated with a profound loss of mitochondrial functions caused by various stress conditions, such as oxidative and metabolic stress, protein folding or import defects, and mitochondrial DNA alteration. Cells engage in different coordinated responses to safeguard mitochondrial homeostasis. In this review, we will explore the contribution of mitochondrial stress responses that are activated by the organelle to perceive these dangerous conditions, keep them under control and rescue the physiological condition of nervous cells. In the sections to come, particular attention will be dedicated to analyzing how compensatory mitochondrial hyperfusion, mitophagy, mitochondrial unfolding protein response, and apoptosis impact human neuronal diseases. Finally, we will discuss the relevance of the new concept: the "mito-inflammation", a mitochondria-mediated inflammatory response that is recently found to cover a relevant role in the pathogenesis of diverse inflammatory-related diseases, including neuronal disorders.
    Language English
    Publishing date 2022-05-17
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.339473
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 758: 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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  10. Article ; Online: The Complex Relationship between Hypoxia Signaling, Mitochondrial Dysfunction and Inflammation in Calcific Aortic Valve Disease: Insights from the Molecular Mechanisms to Therapeutic Approaches.

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

    International journal of molecular sciences

    2023  Volume 24, Issue 13

    Abstract: Calcific aortic valve stenosis (CAVS) is among the most common causes of cardiovascular mortality in an aging population worldwide. The pathomechanisms of CAVS are such a complex and multifactorial process that researchers are still making progress to ... ...

    Abstract Calcific aortic valve stenosis (CAVS) is among the most common causes of cardiovascular mortality in an aging population worldwide. The pathomechanisms of CAVS are such a complex and multifactorial process that researchers are still making progress to understand its physiopathology as well as the complex players involved in CAVS pathogenesis. Currently, there is no successful and effective treatment to prevent or slow down the disease. Surgical and transcatheter valve replacement represents the only option available for treating CAVS. Insufficient oxygen availability (hypoxia) has a critical role in the pathogenesis of almost all CVDs. This process is orchestrated by the hallmark transcription factor, hypoxia-inducible factor 1 alpha subunit (HIF-1α), which plays a pivotal role in regulating various target hypoxic genes and metabolic adaptations. Recent studies have shown a great deal of interest in understanding the contribution of HIF-1α in the pathogenesis of CAVS. However, it is deeply intertwined with other major contributors, including sustained inflammation and mitochondrial impairments, which are attributed primarily to CAVS. The present review aims to cover the latest understanding of the complex interplay effect of hypoxia signaling pathways, mitochondrial dysfunction, and inflammation in CAVS. We propose further hypotheses and interconnections on the complexity of these impacts in a perspective of better understanding the pathophysiology. These interplays will be examined considering recent studies that shall help us better dissect the molecular mechanism to enable the design and development of potential future therapeutic approaches that can prevent or slow down CAVS processes.
    MeSH term(s) Humans ; Aged ; Aortic Valve/pathology ; Aortic Valve Stenosis/pathology ; Inflammation/metabolism ; Hypoxia/metabolism
    Language English
    Publishing date 2023-07-05
    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/ijms241311105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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