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  1. Book ; Online: Gene therapy for renal diseases and transplantation

    Benigni, Ariela

    a survey of potential fields of application

    2008  

    Author's details vol. ed.: Ariela Benigni
    Language English
    Size VIII + 168 S.
    Publisher Karger
    Publishing place Basel
    Publishing country Switzerland
    Document type Book ; Online
    HBZ-ID TT050388147
    ISBN 978-3-8055-8506-4 ; 3-8055-8506-3
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Gene therapy for renal diseases and transplantation

    Benigni, Ariela

    (Contributions to nephrology ; 159)

    2008  

    Author's details vol. ed. Ariela Benigni
    Series title Contributions to nephrology ; 159
    Collection
    Keywords Kidney Diseases / therapy ; Gene Therapy ; Graft Rejection / therapy ; Kidney Transplantation ; Nierenkrankheit ; Gentherapie ; Niere ; Gentransfer ; Nierentransplantation ; Transplantatabstoßung
    Subject Somatische Gentherapie ; Abstoßungsreaktion ; Transplantat ; Niere ; Genübertragung ; Transfer ; Nephros ; Ren ; Nephropathie ; Nierenerkrankung ; Nierenerkrankungen ; Renopathie
    Language English
    Size VIII, 167 S. : Ill., graph. Darst.
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT015542536
    ISBN 978-3-8055-8505-7 ; 3-8055-8505-5
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: Tissue-Resident Macrophages in Solid Organ Transplantation: Harmful or Protective?

    Aiello, Sistiana / Benigni, Ariela / Remuzzi, Giuseppe

    Journal of immunology (Baltimore, Md. : 1950)

    2024  Volume 212, Issue 7, Page(s) 1051–1061

    Abstract: Transplanted organs carry donor immune cells into the recipient, the majority of which are tissue-resident macrophages (TRMs). The role they play in guiding the fate of the transplanted organ toward acceptance or rejection remains elusive. TRMs originate ...

    Abstract Transplanted organs carry donor immune cells into the recipient, the majority of which are tissue-resident macrophages (TRMs). The role they play in guiding the fate of the transplanted organ toward acceptance or rejection remains elusive. TRMs originate from both embryonic and bone marrow-derived precursors. Embryo-derived TRMs retain the embryonic capability to proliferate, so they are able to self-renew and, theoretically, persist for extended periods of time after transplantation. Bone marrow-derived TRMs do not proliferate and must constantly be replenished by adult circulating monocytes. Recent studies have aimed to clarify the different roles and interactions between donor TRMs, recipient monocytes, and monocyte-derived macrophages (MFs) after organ transplantation. This review aims to shed light on how MFs affect the fate of a transplanted organ by differentiating between the role of donor TRMs and that of MFs derived from graft infiltrating monocytes.
    MeSH term(s) Macrophages ; Monocytes ; Organ Transplantation ; Bone Marrow ; Embryo, Mammalian
    Language English
    Publishing date 2024-03-18
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2300625
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Sirtuins in kidney health and disease.

    Perico, Luca / Remuzzi, Giuseppe / Benigni, Ariela

    Nature reviews. Nephrology

    2024  Volume 20, Issue 5, Page(s) 313–329

    Abstract: Sirtuins (SIRTs) are putative regulators of lifespan in model organisms. Since the initial discovery that SIRTs could promote longevity in nematodes and flies, the identification of additional properties of these proteins has led to understanding of ... ...

    Abstract Sirtuins (SIRTs) are putative regulators of lifespan in model organisms. Since the initial discovery that SIRTs could promote longevity in nematodes and flies, the identification of additional properties of these proteins has led to understanding of their roles as exquisite sensors that link metabolic activity to oxidative states. SIRTs have major roles in biological processes that are important in kidney development and physiological functions, including mitochondrial metabolism, oxidative stress, autophagy, DNA repair and inflammation. Furthermore, altered SIRT activity has been implicated in the pathophysiology and progression of acute and chronic kidney diseases, including acute kidney injury, diabetic kidney disease, chronic kidney disease, polycystic kidney disease, autoimmune diseases and renal ageing. The renoprotective roles of SIRTs in these diseases make them attractive therapeutic targets. A number of SIRT-activating compounds have shown beneficial effects in kidney disease models; however, further research is needed to identify novel SIRT-targeting strategies with the potential to treat and/or prevent the progression of kidney diseases and increase the average human healthspan.
    MeSH term(s) Sirtuins/metabolism ; Sirtuins/physiology ; Humans ; Kidney Diseases/metabolism ; Animals ; Kidney/metabolism ; Oxidative Stress ; Renal Insufficiency, Chronic/metabolism ; Mitochondria/metabolism ; Aging/physiology ; Aging/metabolism ; Autophagy/physiology
    Chemical Substances Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2024-02-06
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-024-00806-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Editorial: Women in renal pharmacology: 2021.

    Benigni, Ariela / Tomasoni, Susanna

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 1054354

    Language English
    Publishing date 2022-10-21
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.1054354
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: SARS-CoV-2 and the spike protein in endotheliopathy.

    Perico, Luca / Benigni, Ariela / Remuzzi, Giuseppe

    Trends in microbiology

    2023  Volume 32, Issue 1, Page(s) 53–67

    Abstract: SARS-CoV-2, the causative agent of COVID-19, primarily affects the epithelial compartment in the upper and lower airways. There is evidence that the microvasculature in both the pulmonary and extrapulmonary systems is a major target of SARS-CoV-2. ... ...

    Abstract SARS-CoV-2, the causative agent of COVID-19, primarily affects the epithelial compartment in the upper and lower airways. There is evidence that the microvasculature in both the pulmonary and extrapulmonary systems is a major target of SARS-CoV-2. Consistent with this, vascular dysfunction and thrombosis are the most severe complications in COVID-19. The proinflammatory milieu triggered by the hyperactivation of the immune system by SARS-CoV-2 has been suggested to be the main trigger for endothelial dysfunction during COVID-19. More recently, a rapidly growing number of reports have indicated that SARS-CoV-2 can interact directly with endothelial cells through the spike protein, leading to multiple instances of endothelial dysfunction. Here, we describe all the available findings showing the direct effect of the SARS-CoV-2 spike protein on endothelial cells and offer mechanistic insights into the molecular basis of vascular dysfunction in severe COVID-19.
    MeSH term(s) Humans ; SARS-CoV-2 ; COVID-19/complications ; Spike Glycoprotein, Coronavirus/genetics ; Endothelial Cells/metabolism
    Chemical Substances spike protein, SARS-CoV-2 ; Spike Glycoprotein, Coronavirus
    Language English
    Publishing date 2023-06-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1158963-2
    ISSN 1878-4380 ; 0966-842X
    ISSN (online) 1878-4380
    ISSN 0966-842X
    DOI 10.1016/j.tim.2023.06.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Imaging the Kidney with an Unconventional Scanning Electron Microscopy Technique: Analysis of the Subpodocyte Space in Diabetic Mice.

    Conti, Sara / Remuzzi, Giuseppe / Benigni, Ariela / Tomasoni, Susanna

    International journal of molecular sciences

    2022  Volume 23, Issue 3

    Abstract: Transmission electron microscopy (TEM) remains the gold standard for renal histopathological diagnoses, given its higher resolving power, compared with light microscopy. However, it imposes several limitations on pathologists, including longer sample ... ...

    Abstract Transmission electron microscopy (TEM) remains the gold standard for renal histopathological diagnoses, given its higher resolving power, compared with light microscopy. However, it imposes several limitations on pathologists, including longer sample preparation time and a small observation area. To overcome these, we introduced a scanning electron microscopy (SEM) technique for imaging resin-embedded semi-thin sections of renal tissue. We developed a rapid tissue preparation protocol for experimental models and human biopsies which, alongside SEM digital imaging acquisition of secondary electrons (SE-SEM), enables fast electron microscopy examination, with a resolution similar to that achieved by TEM. We used this unconventional SEM imaging approach to investigate the subpodocyte space (SPS) in BTBR
    MeSH term(s) Animals ; Diabetes Mellitus, Experimental/pathology ; Diabetes Mellitus, Type 2/pathology ; Glomerular Filtration Barrier/ultrastructure ; Mice ; Microscopy, Electron, Scanning ; Podocytes/ultrastructure
    Language English
    Publishing date 2022-02-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23031699
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Angiotensin-converting enzyme 2: from a vasoactive peptide to the gatekeeper of a global pandemic.

    Perico, Luca / Benigni, Ariela / Remuzzi, Giuseppe

    Current opinion in nephrology and hypertension

    2021  Volume 30, Issue 2, Page(s) 252–263

    Abstract: Purpose of review: We provide a comprehensive overview of angiotensin-converting enzyme 2 (ACE2) as a possible candidate for pharmacological approaches to halt inflammatory processes in different pathogenic conditions.: Recent findings: ACE2 has ... ...

    Abstract Purpose of review: We provide a comprehensive overview of angiotensin-converting enzyme 2 (ACE2) as a possible candidate for pharmacological approaches to halt inflammatory processes in different pathogenic conditions.
    Recent findings: ACE2 has quickly gained prominence in basic research as it has been identified as the main entry receptor for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). This novel pathogen causes Coronavirus Disease 2019 (COVID-19), a pathogenic condition that reached pandemic proportion and is associated with unprecedented morbidity and mortality.
    Summary: The renin-angiotensin system is a complex, coordinated hormonal cascade that plays a pivotal role in controlling individual cell behaviour and multiple organ functions. ACE2 acts as an endogenous counter-regulator to the pro-inflammatory and pro-fibrotic pathways triggered by ACE through the conversion of Ang II into the vasodilatory peptide Ang 1-7. We discuss the structure, function and expression of ACE2 in different tissues. We also briefly describe the role of ACE2 as a pivotal driver across a wide spectrum of pathogenic conditions, such as cardiac and renal diseases. Furthermore, we provide the most recent data concerning the possible role of ACE2 in mediating SARS-CoV-2 infection and dictating COVID-19 severity.
    MeSH term(s) Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; COVID-19/enzymology ; Humans ; Renin-Angiotensin System/drug effects ; SARS-CoV-2 ; COVID-19 Drug Treatment
    Chemical Substances Angiotensin-Converting Enzyme Inhibitors ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2021-01-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1151092-4
    ISSN 1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
    ISSN (online) 1473-6543 ; 1535-3842
    ISSN 1062-4813 ; 1062-4821
    DOI 10.1097/MNH.0000000000000692
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The iNADequacy of renal cell metabolism: modulating NAD

    Perico, Luca / Benigni, Ariela

    Kidney international

    2019  Volume 96, Issue 2, Page(s) 264–267

    MeSH term(s) Acute Kidney Injury ; Biosynthetic Pathways ; Humans ; Kidney ; NAD
    Chemical Substances NAD (0U46U6E8UK)
    Language English
    Publishing date 2019-07-19
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2019.03.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Sirt3 deficiency promotes endothelial dysfunction and aggravates renal injury.

    Pezzotta, Anna / Perico, Luca / Corna, Daniela / Morigi, Marina / Remuzzi, Giuseppe / Benigni, Ariela / Imberti, Barbara

    PloS one

    2023  Volume 18, Issue 10, Page(s) e0291909

    Abstract: Sirtuin 3 (SIRT3), the main deacetylase of mitochondria, modulates the acetylation levels of substrates governing metabolism and oxidative stress. In the kidney, we showed that SIRT3 affects the proper functioning of high energy-demanding cells, such as ... ...

    Abstract Sirtuin 3 (SIRT3), the main deacetylase of mitochondria, modulates the acetylation levels of substrates governing metabolism and oxidative stress. In the kidney, we showed that SIRT3 affects the proper functioning of high energy-demanding cells, such as tubular cells and podocytes. Less is known about the role of SIRT3 in regulating endothelial cell function and its impact on the progression of kidney disease. Here, we found that whole body Sirt3-deficient mice exhibited reduced renal capillary density, reflecting endothelial dysfunction, and VEGFA expression compared to wild-type mice. This was paralleled by activation of hypoxia signaling, upregulation of HIF-1α and Angiopietin-2, and oxidative stress increase. These alterations did not result in kidney disease. However, when Sirt3-deficient mice were exposed to the nephrotoxic stimulus Adriamycin (ADR) they developed aggravated endothelial rarefaction, altered VEGFA signaling, and higher oxidative stress compared to wild-type mice receiving ADR. As a result, ADR-treated Sirt3-deficient mice experienced a more severe injury with exacerbated albuminuria, podocyte loss and fibrotic lesions. These data suggest that SIRT3 is a crucial regulator of renal vascular homeostasis and its dysregulation is a predisposing factor for kidney disease. By extension, our findings indicate SIRT3 as a pharmacologic target in progressive renal disease whose treatments are still imperfect.
    MeSH term(s) Mice ; Animals ; Sirtuin 3/metabolism ; Kidney/metabolism ; Oxidative Stress ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Mitochondria/metabolism ; Vascular Diseases/metabolism
    Chemical Substances Sirtuin 3 (EC 3.5.1.-) ; Sirt3 protein, mouse
    Language English
    Publishing date 2023-10-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0291909
    Database MEDical Literature Analysis and Retrieval System OnLINE

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