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  • 1
    Online Resource
    Online Resource
    Activation of BNIP3-mediated mitophagy protects against renal ischemia–reperfusion injury
    Springer Science and Business Media LLC ; 2019
    In:  Cell Death & Disease Vol. 10, No. 9 ( 2019-09-12)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 10, No. 9 ( 2019-09-12)
    Abstract: Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia–reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced OGD-R-induced mitophagy, and potentiated OGD-R-induced cell death. In vivo, Bnip3 knockout worsened renal IR injury, as manifested by more severe renal dysfunction and tissue injury. We further showed that Bnip3 knockout reduced mitophagy, which resulted in the accumulation of damaged mitochondria, increased production of reactive oxygen species, and enhanced cell death and inflammatory response in kidneys following renal IR. Taken together, these findings suggest that BNIP3-mediated mitophagy has a critical role in mitochondrial quality control and tubular cell survival during AKI.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-019-1899-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2541626-1
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  • 2
    Online Resource
    Online Resource
    Phosphorylation by GSK-3β Increases the Stability of SIRT6 to Alleviate TGF-β-Induced Fibrotic Response in Renal Tubular Cells
    Elsevier BV ; 2022
    In:  SSRN Electronic Journal
    Details
    In: SSRN Electronic Journal, Elsevier BV
    Type of Medium: Online Resource
    ISSN: 1556-5068
    URL: Article
    DOI: 10.2139/ssrn.4148154
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
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  • 3
    Online Resource
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    Non-coding RNAs in kidney injury and repair
    American Physiological Society ; 2019
    In:  American Journal of Physiology-Cell Physiology Vol. 317, No. 2 ( 2019-08-01), p. C177-C188
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 317, No. 2 ( 2019-08-01), p. C177-C188
    Abstract: Acute kidney injury (AKI) is a major kidney disease featured by a rapid decline of renal function. Pathologically, AKI is characterized by tubular epithelial cell injury and death. Besides its acute consequence, AKI contributes critically to the development and progression of chronic kidney disease (CKD). After AKI, surviving tubular cells regenerate to repair. Normal repair restores tubular integrity, while maladaptive or incomplete repair results in renal fibrosis and eventually CKD. Non-coding RNAs (ncRNAs) are functional RNA molecules that are transcribed from DNA but not translated into proteins, which mainly include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), small nucleolar RNAs (snoRNAs), and tRNAs. Accumulating evidence suggests that ncRNAs play important roles in kidney injury and repair. In this review, we summarize the recent advances in the understanding of the roles of ncRNAs, especially miRNAs and lncRNAs in kidney injury and repair, discuss the potential application of ncRNAs as biomarkers of AKI as well as therapeutic targets for treating AKI and impeding AKI-CKD transition, and highlight the future research directions of ncRNAs in kidney injury and repair.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00048.2019
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 4
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    Phosphorylation by GSK-3β increases the stability of SIRT6 to alleviate TGF-β-induced fibrotic response in renal tubular cells
    Elsevier BV ; 2022
    In:  Life Sciences Vol. 308 ( 2022-11), p. 120914-
    Details
    In: Life Sciences, Elsevier BV, Vol. 308 ( 2022-11), p. 120914-
    Type of Medium: Online Resource
    ISSN: 0024-3205
    URL: Article
    DOI: 10.1016/j.lfs.2022.120914
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2013911-1
    SSG: 12
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  • 5
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    PACS-2 deficiency in tubular cells aggravates lipid-related kidney injury in diabetic kidney disease
    Springer Science and Business Media LLC ; 2022
    In:  Molecular Medicine Vol. 28, No. 1 ( 2022-12)
    Details
    In: Molecular Medicine, Springer Science and Business Media LLC, Vol. 28, No. 1 ( 2022-12)
    Abstract: Lipid accumulation in tubular cells plays a key role in diabetic kidney disease (DKD). Targeting lipid metabolism disorders has clinical value in delaying the progression of DKD, but the precise mechanism by which molecules mediate lipid-related kidney injury remains unclear. Phosphofurin acidic cluster sorting protein 2 (PACS-2) is a multifunctional sorting protein that plays a role in lipid metabolism. This study determined the role of PACS-2 in lipid-related kidney injury in DKD. Methods Diabetes was induced by a high-fat diet combined with intraperitoneal injections of streptozotocin (HFD/STZ) in proximal tubule-specific knockout of Pacs-2 mice ( PT - Pacs-2 −/− mice) and the control mice ( Pacs-2 fl/fl mice). Transcriptomic analysis was performed between Pacs-2 fl/fl mice and PT - Pacs-2 −/− mice. Results Diabetic PT - Pacs-2 −/− mice developed more severe tubule injury and proteinuria compared to diabetic Pacs-2 fl/fl mice, which accompanied with increasing lipid synthesis, uptake and decreasing cholesterol efflux as well as lipid accumulation in tubules of the kidney. Furthermore, transcriptome analysis showed that the mRNA level of sterol O -acyltransferase 1 ( Soat1 ) was up-regulated in the kidney of control PT - Pacs-2 −/− mice . Transfection of HK2 cells with PACS-2 siRNA under high glucose plus palmitic acid (HGPA) condition aggravated lipid deposition and increased the expression of SOAT1 and sterol regulatory element-binding proteins (SREBPs), while the effect was blocked partially in that of co-transfection of SOAT1 siRNA. Conclusions PACS-2 has a protective role against lipid-related kidney injury in DKD through SOAT1/SREBPs signaling.
    Type of Medium: Online Resource
    ISSN: 1076-1551 , 1528-3658
    URL: Article
    DOI: 10.1186/s10020-022-00545-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1475577-4
    detail.hit.zdb_id: 1283676-X
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  • 6
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    DataSheet_1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-7-7)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-7-7)
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.925738
    DOI: 10.3389/fimmu.2022.925738.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 7
    Online Resource
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    Nicotinamide reduces renal interstitial fibrosis by suppressing tubular injury and inflammation
    Wiley ; 2019
    In:  Journal of Cellular and Molecular Medicine Vol. 23, No. 6 ( 2019-06), p. 3995-4004
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 23, No. 6 ( 2019-06), p. 3995-4004
    Abstract: Renal interstitial fibrosis is a common pathological feature in progressive kidney diseases currently lacking effective treatment. Nicotinamide (NAM), a member of water‐soluble vitamin B family, was recently suggested to have a therapeutic potential for acute kidney injury (AKI) in mice and humans. The effect of NAM on chronic kidney pathologies, including renal fibrosis, is unknown. Here we have tested the effects of NAM on renal interstitial fibrosis using in vivo and in vitro models. In vivo, unilateral urethral obstruction (UUO) induced renal interstitial fibrosis as indicated Masson trichrome staining and expression of pro‐fibrotic proteins, which was inhibited by NAM. In UUO, NAM suppressed tubular atrophy and apoptosis. In addition, NAM suppressed UUO‐associated T cell and macrophage infiltration and induction of pro‐inflammatory cytokines, such as TNF‐α and IL‐1β. In cultured mouse proximal tubule cells, NAM blocked TGF–β‐induced expression of fibrotic proteins, while it marginally suppressed the morphological changes induced by TGF‐β. NAM also suppressed the expression of pro‐inflammatory cytokines (eg MCP‐1 and IL‐1β) during TGF‐β treatment of these cells. Collectively, the results demonstrate an anti‐fibrotic effect of NAM in kidneys, which may involve the suppression of tubular injury and inflammation.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2019.23.issue-6
    DOI: 10.1111/jcmm.14285
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2076114-4
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  • 8
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    Online Resource
    PARK7 is induced to protect against endotoxic acute kidney injury by suppressing NF-κB
    Portland Press Ltd. ; 2022
    In:  Clinical Science Vol. 136, No. 24 ( 2022-12-22), p. 1877-1891
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 136, No. 24 ( 2022-12-22), p. 1877-1891
    Abstract: Sepsis is a leading cause of acute kidney injury (AKI), and the pathogenesis of septic AKI remains largely unclear. Parkinson disease protein 7 (PARK7) is a protein of multiple functions that was recently implicated in septic AKI, but the underlying mechanism is unknown. In the present study, we determined the role of PARK7 in septic AKI and further explored the underlying mechanism in lipopolysaccharide (LPS)-induced endotoxic models. PARK7 was induced both in vivo and in vitro following LPS treatment. Compared with wild-type (WT) mice, Park7-deficient mice experienced aggravated kidney tissue damage and dysfunction, and enhanced tubular apoptosis and inflammation following LPS treatment. Consistently, LPS-induced apoptosis and inflammation in renal tubular cells in vitro were exacerbated by Park7 knockdown, whereas they were alleviated by PARK7 overexpression. Mechanistically, silencing Park7 facilitated nuclear translocation and phosphorylation of p65 (a key component of the nuclear factor kappa B [NF-κB] complex) during LPS treatment, whereas PARK7 overexpression partially prevented these changes. Moreover, we detected PARK7 interaction with p65 in the cytoplasm in renal tubular cells, which was enhanced by LPS treatment. Collectively, these findings suggest that PARK7 is induced to protect against septic AKI through suppressing NF-κB signaling.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20220493
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2022
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  • 9
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    Online Resource
    Mitophagy in Acute Kidney Injury and Kidney Repair
    MDPI AG ; 2020
    In:  Cells Vol. 9, No. 2 ( 2020-02-01), p. 338-
    Details
    In: Cells, MDPI AG, Vol. 9, No. 2 ( 2020-02-01), p. 338-
    Abstract: Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules after severe or episodic AKI leads to renal fibrosis and, eventually, CKD. Recent studies highlight a key role of mitochondrial pathology in AKI development and abnormal kidney repair after AKI. As such, timely elimination of damaged mitochondria in renal tubular cells represents an important quality control mechanism for cell homeostasis and survival during kidney injury and repair. Mitophagy is a selective form of autophagy that selectively removes redundant or damaged mitochondria. Here, we summarize our recent understanding on the molecular mechanisms of mitophagy, discuss the role of mitophagy in AKI development and kidney repair after AKI, and present future research directions and therapeutic potential.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells9020338
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2661518-6
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  • 10
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    Serum sclerostin in vascular calcification and clinical outcome in chronic kidney disease
    SAGE Publications ; 2018
    In:  Diabetes and Vascular Disease Research Vol. 15, No. 2 ( 2018-03), p. 99-105
    Details
    In: Diabetes and Vascular Disease Research, SAGE Publications, Vol. 15, No. 2 ( 2018-03), p. 99-105
    Type of Medium: Online Resource
    ISSN: 1479-1641 , 1752-8984
    URL: Article
    DOI: 10.1177/1479164117742316
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
    detail.hit.zdb_id: 2250797-8
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