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  • Unbekannt  (7)
  • 1
    Online-Ressource
    Online-Ressource
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-7-7)
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-7-7)
    Kurzfassung: Chronic inflammation contributes to maladaptive kidney repair, but its regulation is unclear. Here, we report that sirtuin 1 (SIRT1) is downregulated after repeated low-dose cisplatin (RLDC) injury, and this downregulation leads to p65 acetylation and consequent NF-κB activation resulting in a persistent inflammatory response. RLDC induced the down-regulation of SIRT1 and activation of NF-κB, which were accompanied by chronic tubular damage, tubulointerstitial inflammation, and fibrosis in mice. Inhibition of NF-κB suppressed the production of pro-inflammatory cytokines and fibrotic phenotypes in RLDC-treated renal tubular cells. SIRT1 activation by its agonists markedly reduced the acetylation of p65 (a key component of NF-κB), resulting in the attenuation of the inflammatory and fibrotic responses. Conversely, knockdown of SIRT1 exacerbated these cellular changes. At the upstream, p53 was activated after RLDC treatment to repress SIRT1, resulting in p65 acetylation, NF-κB activation and transcription of inflammatory cytokines. In mice, SIRT1 agonists attenuated RLDC-induced chronic inflammation, tissue damage, and renal fibrosis. Together, these results unveil the p53/SIRT1/NF-κB signaling axis in maladaptive kidney repair following RLDC treatment, where p53 represses SIRT1 to increase p65 acetylation for NF-κB activation, leading to chronic renal inflammation.
    Materialart: Online-Ressource
    ISSN: 1664-3224
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2022
    ZDB Id: 2606827-8
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    Frontiers Media SA ; 2022
    In:  Frontiers in Chemistry Vol. 10 ( 2022-12-5)
    In: Frontiers in Chemistry, Frontiers Media SA, Vol. 10 ( 2022-12-5)
    Kurzfassung: Dynamic fluorophore 9,14-diphenyl-9,14-dihydrodibenzo[a,c]phenazine (DPAC) affords a new platform to produce diverse emission outputs. In this paper, a novel DPAC-containing crown ether macrocycle D-6 is synthesized and characterized. Host-guest interactions of D-6 with different ammonium guests produced a variety of fluorescence with hypsochromic shifts up to 130 nm, which are found to be affected by choice of solvent or guest and host/guest stoichiometry. Formation of supramolecular complexes were confirmed by UV-vis titration, 1 H NMR and HRMS spectroscopy.
    Materialart: Online-Ressource
    ISSN: 2296-2646
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2022
    ZDB Id: 2711776-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    In: Frontiers in Aging Neuroscience, Frontiers Media SA, Vol. 15 ( 2023-3-28)
    Kurzfassung: Older adults oftentimes suffer from the conditions in multiple physiologic systems, interfering with their daily function and thus contributing to physical frailty. The contributions of such multisystem conditions to physical frailty have not been well characterized. Methods In this study, 442 (mean age = 71.4 ± 8.1 years, 235 women) participants completed the assessment of frailty syndromes, including unintentional weight loss, exhaustion, slowness, low activity, and weakness, and were categorized into frail (≥3 conditions), pre-frail (1 or 2 conditions), and robust (no condition) status. Multisystem conditions including cardiovascular diseases, vascular function, hypertension, diabetes, sleep disorders, sarcopenia, cognitive impairment, and chronic pain were assessed. Structural equation modeling examined the interrelationships between these conditions and their associations with frailty syndromes. Results Fifty (11.3%) participants were frail, 212 (48.0%) were pre-frail, and 180 (40.7%) were robust. We observed that worse vascular function was directly associated with higher risk of slowness [standardized coefficient (SC) = −0.419, p & lt; 0.001], weakness (SC = −0.367, p & lt; 0.001), and exhaustion (SC = −0.347, p & lt; 0.001). Sarcopenia was associated with both slowness (SC = 0.132, p = 0.011) and weakness (SC = 0.217, p = 0.001). Chronic pain, poor sleep quality, and cognitive impairment were associated with exhaustion (SC = 0.263, p & lt; 0.001; SC = 0.143, p = 0.016; SC = 0.178, p = 0.004, respectively). The multinomial logistic regression showed that greater number of these conditions were associated with increased probability of being frail (odds ratio & gt;1.23, p & lt; 0.032). Conclusion These findings in this pilot study provide novel insights into how multisystem conditions are associated with each other and with frailty in older adults. Future longitudinal studies are warranted to explore how the changes in these health conditions alter frailty status.
    Materialart: Online-Ressource
    ISSN: 1663-4365
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2023
    ZDB Id: 2558898-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    IOP Publishing ; 2023
    In:  Chinese Physics Letters Vol. 40, No. 8 ( 2023-08-01), p. 087103-
    In: Chinese Physics Letters, IOP Publishing, Vol. 40, No. 8 ( 2023-08-01), p. 087103-
    Kurzfassung: The duality between electric and magnetic dipoles inspires recent comparisons between ferronics and magnonics. Here we predict surface polarization waves or “ferrons” in ferroelectric insulators, taking the long-range dipolar interaction into account. We predict properties that are strikingly different from the magnetic counterpart, i.e. the surface Damon–Eshbach magnons in ferromagnets. The dipolar interaction pushes the ferron branch with locked circular polarization and momentum to the ionic plasma frequency. The low-frequency modes are on the other hand in-plane polarized normal to their wave vectors. The strong anisotropy of the lower branch renders directional emissions of electric polarization and chiral near fields when activated by a focused laser beam, allowing optical routing in ferroelectric devices.
    Materialart: Online-Ressource
    ISSN: 0256-307X , 1741-3540
    Sprache: Unbekannt
    Verlag: IOP Publishing
    Publikationsdatum: 2023
    ZDB Id: 2040565-0
    SSG: 6,25
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-5-30)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-5-30)
    Kurzfassung: Autophagy, a highly conserved catabolic pathway in eukaryotic cells, contributes to the maintenance of the homeostasis and function of the kidney. Upon acute kidney injury (AKI), autophagy is activated in renal tubular cells to act as an intrinsic protective mechanism. However, the role of autophagy in the development of chronic kidney pathologies including renal fibrosis after AKI remains unclear. In this study, we detected a persistent autophagy activation in mouse kidneys after nephrotoxicity of repeated low dose cisplatin (RLDC) treatment. 3-methyladenine (3-MA) and chloroquine (CQ), respective inhibitors of autophagy at the initiation and degradation stages, blocked autophagic flux and improved kidney repair in post-RLDC mice, as indicated by kidney weight, renal function, and less interstitial fibrosis. In vitro , RLDC induced a pro-fibrotic phenotype in renal tubular cells, including the production and secretion of pro-fibrotic cytokines. Notably, autophagy inhibitors blocked RLDC-induced secretion of pro-fibrotic cytokines in these cells. Together, the results indicate that persistent autophagy after AKI induces pro-fibrotic cytokines in renal tubular cells, promoting renal fibrosis and chronic kidney disease.
    Materialart: Online-Ressource
    ISSN: 1663-9812
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2022
    ZDB Id: 2587355-6
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-5-21)
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-5-21)
    Kurzfassung: Renal fibrosis is the final common pathway to chronic kidney diseases regardless of etiology. Parkinson disease protein 7 (PARK7) is a multifunctional protein involved in various cellular processes, but its pathophysiological role in kidneys remain largely unknown. Here, we have determined the role of PARK7 in renal fibrosis and have further elucidated the underlying mechanisms by using the in vivo mouse model of unilateral ureteric obstruction (UUO) and the in vitro model of transforming growth factor-b (TGFB1) treatment of cultured kidney proximal tubular cells. PARK7 decreased markedly in atrophic kidney tubules in UUO mice, and Park7 deficiency aggravated UUO-induced renal fibrosis, tubular cell apoptosis, ROS production and inflammation. In vitro , TGFB1 treatment induced fibrotic changes in renal tubular cells, which was accompanied by alterations of PARK7. Park7 knockdown exacerbated TGFB1-induced fibrotic changes, cell apoptosis and ROS production, whereas Park7 overexpression or treatment with ND-13 (a PARK7-derived peptide) attenuated these TGFB1-induced changes. Mechanistically, PARK7 translocated into the nucleus of renal tubular cells following TGFB1 treatment or UUO, where it induced the expression of SOD2, an antioxidant enzyme. Taken together, these results indicate that PARK7 protects against chronic kidney injury and renal fibrosis by inducing SOD2 to reduce oxidative stress in tubular cells.
    Materialart: Online-Ressource
    ISSN: 1664-3224
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2021
    ZDB Id: 2606827-8
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    Frontiers Media SA ; 2020
    In:  Frontiers in Physiology Vol. 11 ( 2020-12-17)
    In: Frontiers in Physiology, Frontiers Media SA, Vol. 11 ( 2020-12-17)
    Kurzfassung: Autophagy is a conserved, multistep pathway that degrades and recycles dysfunctional organelles and macromolecules to maintain cellular homeostasis. Mammalian target of rapamycin (mTOR) and adenosine-monophosphate activated-protein kinase (AMPK) are major negative and positive regulators of autophagy, respectively. In cisplatin-induced acute kidney injury (AKI) or nephrotoxicity, autophagy is rapidly induced in renal tubular epithelial cells and acts as a cytoprotective mechanism for cell survival. Both mTOR and AMPK have been implicated in the regulation of autophagy in cisplatin-induced AKI. Targeting mTOR and/or AMPK may offer effective strategies for kidney protection during cisplatin-mediated chemotherapy.
    Materialart: Online-Ressource
    ISSN: 1664-042X
    Sprache: Unbekannt
    Verlag: Frontiers Media SA
    Publikationsdatum: 2020
    ZDB Id: 2564217-0
    Standort Signatur Einschränkungen Verfügbarkeit
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