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  • 1
    Online Resource
    Online Resource
    Aversion to a High Salt Taste is Disturbed in Patients With CKD
    Elsevier BV ; 2024
    In:  Kidney International Reports Vol. 9, No. 5 ( 2024-05), p. 1254-1264
    Details
    In: Kidney International Reports, Elsevier BV, Vol. 9, No. 5 ( 2024-05), p. 1254-1264
    Type of Medium: Online Resource
    ISSN: 2468-0249
    URL: Article
    DOI: 10.1016/j.ekir.2024.02.1393
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 2887223-X
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  • 2
    Online Resource
    Online Resource
    Streptozotocin induces renal proximal tubular injury through p53 signaling activation
    Springer Science and Business Media LLC ; 2023
    In:  Scientific Reports Vol. 13, No. 1 ( 2023-05-29)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2023-05-29)
    Abstract: Streptozotocin (STZ), an anti-cancer drug that is primarily used to treat neuroendocrine tumors (NETs) in clinical settings, is incorporated into pancreatic β-cells or proximal tubular epithelial cells through the glucose transporter, GLUT2. However, its cytotoxic effects on kidney cells have been underestimated and the underlying mechanisms remain unclear. We herein demonstrated that DNA damage and subsequent p53 signaling were responsible for the development of STZ-induced tubular epithelial injury. We detected tubular epithelial DNA damage in NET patients treated with STZ. Unbiased transcriptomics of STZ-treated tubular epithelial cells in vitro showed the activation of the p53 signaling pathway. STZ induced DNA damage and activated p53 signaling in vivo in a dose-dependent manner, resulting in reduced membrane transporters. The pharmacological inhibition of p53 and sodium-glucose transporter 2 (SGLT2) mitigated STZ-induced epithelial injury. However, the cytotoxic effects of STZ on pancreatic β-cells were preserved in SGLT2 inhibitor-treated mice. The present results demonstrate the proximal tubular-specific cytotoxicity of STZ and the underlying mechanisms in vivo. Since the cytotoxic effects of STZ against β-cells were not impaired by dapagliflozin, pretreatment with an SGLT2 inhibitor has potential as a preventative remedy for kidney injury in NET patients treated with STZ.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-023-35850-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2615211-3
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  • 3
    Online Resource
    Online Resource
    Lower blood pressure and risk of cisplatin nephrotoxicity: a retrospective cohort study
    Springer Science and Business Media LLC ; 2017
    In:  BMC Cancer Vol. 17, No. 1 ( 2017-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 17, No. 1 ( 2017-12)
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/s12885-017-3135-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2041352-X
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  • 4
    Online Resource
    Online Resource
    Abstract 563: Cardiac TIGAR Reduces Myocardial Energetics and Cardiac Functionin the Pressure Overload Heart Failure Model
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Abstract: Background: Although metabolic alterations were observed in heart failure (HF), only recently have the mechanisms underlying these changes been identified. Tumor suppressor p53 responds to metabolic changes thorough several mechanisms. One of the p53 targets, TIGAR (TP53-induced glycolysis and apoptosis regulator) reduces glycolysis and suppresses autophagy, which augments ischemic damage, however its role on HF is unclear. Method and Results: In order to investigate TIGAR’s function in HF, we compared myocardial metabolic and functional outcomes between TIGAR deficient (TIGAR–/–) mice and wild-type (TIGAR+/+) mice subjected to chronic thoracic transverse aortic constriction (TAC), a pressure-overload HF model. In wild-type mice hearts, p53 and TIGAR increased markedly during HF development. Eight weeks after TAC surgery, the left ventricular (LV) dysfunction, fibrosis, oxidative damage, and myocyte apoptosis were significantly advanced in wild-type than in TIGAR–/– mouse heart. Further, myocardial high-energy phosphates in wild-type hearts were significantly decreased compared to those of TIGAR–/– mouse heart. Glucose oxidation and glycolysis rates were also reduced in isolated perfused wild-type hearts following TAC than those in TIGAR–/– hearts, which suggest that the upregulation of TIGAR in HF causes impaired myocardial energetics and function. The effects of TIGAR knockout on LV function were also replicated in tamoxifen (TAM)-inducible cardiac-specific TIGAR knockout mice (TIGARflox/flox/ Tg(Myh6-cre/Esr1) mice). Conclusion: The ablation of TIGAR during pressure-overload HF preserves myocardial function and energetics. Thus, cardiac TIGAR targeted therapy to increase glucose metabolism will be a novel strategy for HF.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.563
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 5
    Online Resource
    Online Resource
    Abstract 295: Genome-wide CRISPR Screen Identifies Keap1-Nrf2 Pathway as a Crucial Regulator for Fibrosis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Research Vol. 127, No. Suppl_1 ( 2020-07-31)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 127, No. Suppl_1 ( 2020-07-31)
    Abstract: Cardiac fibrosis is the pathological feature of myocardial remodeling and clinically involved in various cardiovascular diseases including heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation. Accumulating evidence revealed the molecular mechanism behind organ fibrosis, however, no effective anti-fibrotic therapy has been developed. To find novel anti-fibrotic molecular targets, we performed genome-wide CRISPR library screening with focus on myofibroblast activation. Since a feedforward autocrine loop accelerates myofibroblast differentiation, we employed connective tissue growth factor (CTGF), a center of profibrotic secretome, as a target factor for screening assay. We firstly generated a CTGF-GFP knock-in reporter cell in mesenchymal progenitor cells. The reporter cells were transduced with lentivirus CRISPR library and treated with TGF beta, then high and low GFP signal cells were sorted and sequenced. This screening showed that Keap1-NRF2 pathway was one of the top hits and a novel regulator for CTGF expression. Keap1 knockout attenuated TGF beta-mediated CTGF expression and additional NRF2 knockout cancelled it. Keap1-NRF2 pathway also regulated broadly other profibrotic factors, alpha SMA, periostin, and fibronectin. An activator of NRF2, CDDO-Im treatment had similar effect on TGF beta-mediated profibrotic response. CTGF knockout had little effect on these profibrotic factors, indicating that Keap1-NRF2 is better therapeutic target, as compared with CTGF. Keap1-NRF2 originally reported as a transcriptional regulator for antioxidant and detoxification genes. In silico analysis indicates CTFG promoter has NRF2 response element and ChiP-qPCR experiment confirmed that NRF2 directly regulated CTFG transcriptional expression, not indirectly through antioxidant gene expression. In conclusion, genome-wide screening identified Keap1-NRF2 pathway as a crucial regulator for myofibroblast activation and NRF2 activation might be novel therapy for fibrosis-related diseases.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.127.suppl_1.295
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Abstract 12861: Adjoining Myofibroblasts Disrupt Impulse Propagation of Myocardial Tissue via Connexin 43-Mediated Heterocellular Gap Junctional Coupling
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: The composite population of myofibroblasts (MFBs) and cardiomyocytes (CMCs) is known to alter impulse conduction in the heart. A previous study reported that structural disruption between cardiomyocytes by fibrosis or myofibroblast proliferation causes conduction delay due to insulating or reducing the intercellular current. However, it is unknown whether and how the conduction is altered when the myocardial tissue faces adjoining with MFB-rich granulation tissue, like, e.g. , the border zone of myocardial infarcts during infarct healing. Objectives: To clarify the influence of heterocellular gap-junctional coupling between CMCs and MFBs by calcium imaging in an injured myocardial tissue-mimicking model in which CMCs connect with MFBs via microporous membranes. Methods: Fluo-8 fluorescence patterns of impulse propagation were spatiotemporally imaged (27 x 18.9 mm, 333 frames/s, 32 °C) in neonatal rat CMC monolayers cultured on the upper sides of the Boyden chamber (pore diameter, 8 μm) of which MFB monolayer was co-cultured on the reverse sides (CMC-MFB group). For comparison, CMC monolayers were cultured on both membrane sides (CMC-CMC group). Results: During consecutive pacing at 1 - 4 Hz, CMC monolayers showed concentric propagation from the pacing site with slower conduction velocity (CV) and more irregular wavefronts in a frequency-dependent manner. The conduction slowing and its non-uniformity were more remarkable in the CMC-MFB group than in the CMC-CMC group. We confirmed the gap junction coupling between the upper CMC and lower MFB layers using co-immunostaining and calcein staining. Heptanol, gap junction inhibiter, inhibited calcein dye transfer from the upper CMC layer to the lower MFB layer. The knockdown of Cx43 in MFBs on the reverse layer improved the delay of CV and non-uniformity in the CMC-MFB group. Conclusions: In this study, we clarified the electric association between adjoining MFBs and CMCs. Our observations suggest that adjoining MFBs slow down conduction velocity and disrupt conduction uniformity on CMCs via Cx43-mediated heterocellular gap-junctional coupling between CMCs and MFBs.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.12861
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Abstract 14833: Senescent Endothelial Cells Are Highly Susceptible to SARS-CoV-2 Infection, Which Might Account for the Aggravation of COVID-19 in the Elderly
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Introduction: The pandemic of coronavirus disease 2019 (COVID-19), induced by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has posed a global health emergency. COVID-19 vaccines are certainly effective to prevent infection, severe disease, and hospitalization; however, its spreading remains to be uncontrolled worldwide. The striking feature of COVID-19 is the high mortality in the elderly; every 1,000 people infected with SARS-CoV-2, around 116 will die if they are mid-seventies or older, while little will die if they are under the age of 50. Though elderly is more fragile than younger people in general, this substantial difference in mortality strongly suggest a specific factor(s) that aggravate the disease in elder people. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Hypothesis: Senescent endothelial cells are highly susceptible to SARS-CoV-2 infection. Methods: We experimentally investigated the SARS-CoV-2 infection in ECs, and performed a comparative analysis for post-infection molecular events using young and replicative senescent ECs. Results: We identify that; 1) SARS-CoV-2 infects ECs largely through endocytosis, 2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, possibly through enhanced caveolae-mediated endocytosis, 3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, 4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in young ECs, which might causes further exacerbated dysfunction in senescent ECs, 5) SARS-CoV-2 infection significantly affected coagulation cascade only in senescent ECs. Conclusions: These data strongly suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.14833
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    Abstract 13491: Spermidine Improves Angiogenic Capacity in Senescent Endothelial Cells and Enhances Ischemia Induced Neovascularization in Aged Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Aging is closely associated with high morbidity and mortality of various diseasesincluding cardiovascular disease. Cellular senescence has been cruciallyinvolved in the mechanisms underlying age-related diseases, and vascularendothelial cells 〈 ECs 〉 become senescent during aging. Spermidine, a naturallyoccurring polyamine, is an emerging organic compound that shows various anti-aging effects. Serum spermidine concentration decreases during aging inhuman, and dietary spermidine has been reported to extend healthy lifespanand delay the age-related decline in cognitive and physical performance inmany species such as yeast, worms, flies, and mice. Here, we explored aneffect of spermidine on age-associated decline in angiogenesis. Replicativesenescent ECs were prepared by culturing human ECs for an extended perioduntil passage 18-20, and cellular senescence was confirmed by loss ofproliferation capacity, increased CDK inhibitors expression, and senescence-associated beta-Gal activity. Intracellular polyamine contents were significantlyreduced in replicative senescent ECs, which was recovered by spermidinesupplementation. Spermidine supplementation improved the declinedangiogenic capacities including tube-formation on Matrigel in senescent ECs,while senescence features such as reduced proliferation and senescence-associated beta-Gal activity were not affected. Mechanistically, spermidinesupplementation accelerated the static autophagy flux, and improvedmitochondrial quality, e.g. reduced mitochondrial ROS and preservedmitochondrial membrane potential, in senescent ECs. Ischemia-inducedneovascularization was assessed using the hind-limb ischemia model in youngand aged mice. Blood flow recovery and neovascularization in ischemic musclewere considerably impaired in aged mice comparing to those in young mice. Ofnote, dietary spermidine significantly enhanced ischemia-induced angiogenesis,and improved the blood flow recovery in the ischemic limb, especially in agedmice. Our results reveal new mechanistic insights in anti-aging property ofspermidine, and suggest its therapeutic potential against ischemiccardiovascular disease, particularly in elderly population.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.13491
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 9
    Online Resource
    Online Resource
    Recapture failure in transcatheter aortic valve replacement with CoreValve Evolut R
    Wiley ; 2021
    In:  Catheterization and Cardiovascular Interventions Vol. 98, No. 3 ( 2021-09)
    Details
    In: Catheterization and Cardiovascular Interventions, Wiley, Vol. 98, No. 3 ( 2021-09)
    Abstract: Self‐expanding prostheses for transcatheter aortic valve replacement (TAVR), which can be recaptured, provide us the option of repositioning for a more accurate placement. We report a very rare case in which the recapture of CoreValve Evolut R (Medtronic, Minneapolis, Minnesota) to correct the implantation depth during the deployment could not be achieved. We planned TAVR with a 23 mm Evolut R prosthesis for a 92‐year‐old female with severe aortic stenosis and tightly bent thoracic aorta. During the first deployment attempt, the implantation depth was greater than we expected at 2/3 deployment. They tried to recapture and reposition the prosthesis, but the prosthesis was not re‐sheathed into the capsule of the delivery system. The prosthesis could not be recaptured despite a repeat attempt, and they were forced to deploy the device as it was. The prosthesis was deployed very carefully and implanted successfully without a pop‐up into the ascending aorta. At a later date, this situation was replicated in vitro and was found that the distal segment of the capsule became deformed, increasing the resistance to rotating the grip handle.
    Type of Medium: Online Resource
    ISSN: 1522-1946 , 1522-726X
    URL: Issue
    URL: Article
    DOI: 10.1002/ccd.v98.3
    DOI: 10.1002/ccd.29580
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2001555-0
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  • 10
    Online Resource
    Online Resource
    Cavin-2/SDPR in cardiac fibroblasts regulates cardiac fibrosis and function via TGF-β/Smad signaling in pressure-overloaded hearts
    Elsevier BV ; 2020
    In:  Journal of Molecular and Cellular Cardiology Vol. 140 ( 2020-03), p. 17-
    Details
    In: Journal of Molecular and Cellular Cardiology, Elsevier BV, Vol. 140 ( 2020-03), p. 17-
    Type of Medium: Online Resource
    ISSN: 0022-2828
    URL: Article
    DOI: 10.1016/j.yjmcc.2019.11.038
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 1469767-1
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