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  1. Article ; Online: An enigma: does a high-protein diet accelerate renal damage in humans? Lessons from diabetic animal models.

    Zhan, Ming / Kanwar, Yashpal S

    American journal of physiology. Renal physiology

    2020  Volume 318, Issue 4, Page(s) F979–F981

    MeSH term(s) Animals ; Diabetes Mellitus ; Diabetic Nephropathies ; Diet, High-Protein ; Humans ; Kidney ; Mice ; Models, Animal
    Language English
    Publishing date 2020-03-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00076.2020
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  2. Article ; Online: Aging and Diabetic Kidney Disease: Emerging Pathogenetic Mechanisms and Clinical Implications.

    Chen, Yi / Kanwar, Yashpal S / Chen, Xueqin / Zhan, Ming

    Current medicinal chemistry

    2023  Volume 31, Issue 6, Page(s) 697–725

    Abstract: Diabetic kidney disease (DKD) is one of the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide. With the overpowering trend of aging, the prevalence of DKD in the elderly is progressively increasing. Genetic ... ...

    Abstract Diabetic kidney disease (DKD) is one of the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide. With the overpowering trend of aging, the prevalence of DKD in the elderly is progressively increasing. Genetic factors, abnormal glucose metabolism, inflammation, mitochondrial dysregulation, and oxidative stress all contribute to the development of DKD. Conceivably, during aging, these pathobiological processes are likely to be intensified, and this would further exacerbate the deterioration of renal functions in elderly patients, ultimately leading to ESRD. Currently, the pathogenesis of DKD in the elderly is not very well-understood. This study describes an appraisal of the relationship between diabetic nephropathy and aging while discussing the structural and functional changes in the aged kidney, the impact of related mechanisms on the outcome of DKD, and the latest advances in targeted therapies.
    Language English
    Publishing date 2023-07-04
    Publishing country United Arab Emirates
    Document type Journal Article
    ZDB-ID 1319315-6
    ISSN 1875-533X ; 0929-8673
    ISSN (online) 1875-533X
    ISSN 0929-8673
    DOI 10.2174/0929867330666230621112215
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  3. Article ; Online: Myo

    Zheng, Xiaoping / Deng, Fei / Sharma, Isha / Kanwar, Yashpal S

    American journal of physiology. Renal physiology

    2022  Volume 322, Issue 3, Page(s) F344–F359

    Abstract: Conceivably, like other forms of acute kidney injury, cadmium-induced renal injury may also be associated with oxidative stress and various forms of cell death, including necroptosis, a form of regulated necrosis-associated cell death. ...

    Abstract Conceivably, like other forms of acute kidney injury, cadmium-induced renal injury may also be associated with oxidative stress and various forms of cell death, including necroptosis, a form of regulated necrosis-associated cell death.
    MeSH term(s) Acute Kidney Injury/chemically induced ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Animals ; Cadmium/metabolism ; Cadmium/toxicity ; Female ; Humans ; Inositol Oxygenase/genetics ; Inositol Oxygenase/metabolism ; Kidney/metabolism ; Male ; Mice ; Necroptosis ; Oxidants
    Chemical Substances Oxidants ; Cadmium (00BH33GNGH) ; Inositol Oxygenase (EC 1.13.99.1)
    Language English
    Publishing date 2022-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00460.2021
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  4. Article ; Online: PRMT4 interacts with NCOA4 to inhibit ferritinophagy in cisplatin-induced acute kidney injury.

    Zhou, Lizhi / Deng, Zebin / Wang, Yilong / Zhang, Hao / Yan, Shu / Kanwar, Yashpal S / Wang, Yinhuai / Dai, Yingbo / Deng, Fei

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2024  Volume 38, Issue 7, Page(s) e23584

    Abstract: Cisplatin-induced acute kidney injury (AKI) is commonly seen in the clinical practice, and ferroptosis, a type of non-apoptotic cell death, plays a pivotal role in it. Previous studies suggested that protein arginine methyltransferase 4 (PRMT4) was ... ...

    Abstract Cisplatin-induced acute kidney injury (AKI) is commonly seen in the clinical practice, and ferroptosis, a type of non-apoptotic cell death, plays a pivotal role in it. Previous studies suggested that protein arginine methyltransferase 4 (PRMT4) was incorporated in various bioprocesses, but its role in renal injuries has not been investigated. Our present study showed that PRMT4 was highly expressed in renal proximal tubular cells, and it was downregulated in cisplatin-induced AKI. Besides, genetic disruption of PRMT4 exacerbated, while its overexpression attenuated, cisplatin-induced redox injuries in renal proximal epithelia. Mechanistically, our work showed that PRMT4 interacted with NCOA4 to inhibit ferritinophagy, a type of selective autophagy favoring lipid peroxidation to accelerate ferroptosis. Taken together, our study demonstrated that PRMT4 interacted with NCOA4 to attenuate ferroptosis in cisplatin-induced AKI, suggesting that PRMT4 might present as a new therapeutic target for cisplatin-related nephropathy.
    MeSH term(s) Humans ; Cisplatin/adverse effects ; Acute Kidney Injury/chemically induced ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Kidney/metabolism ; Transcription Factors/metabolism ; Autophagy ; Nuclear Receptor Coactivators/genetics ; Nuclear Receptor Coactivators/metabolism
    Chemical Substances Cisplatin (Q20Q21Q62J) ; Transcription Factors ; NCOA4 protein, human ; Nuclear Receptor Coactivators
    Language English
    Publishing date 2024-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202302596R
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    Zs.MO 296: Show issues

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  5. Article ; Online: Continuum of historical controversies regarding the structural-functional relationship of the glomerular ultrafiltration unit.

    Kanwar, Yashpal S

    American journal of physiology. Renal physiology

    2015  Volume 308, Issue 5, Page(s) F420–4

    MeSH term(s) Animals ; Glomerular Filtration Barrier/drug effects ; Heparin Antagonists/toxicity ; Hyaluronoglucosaminidase/toxicity ; Male ; Protamines/toxicity
    Chemical Substances Heparin Antagonists ; Protamines ; Hyaluronoglucosaminidase (EC 3.2.1.35)
    Language English
    Publishing date 2015-03-01
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00640.2014
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  6. Article ; Online: Myo

    Qi, Huiyue / Deng, Fei / Wang, Yinghuai / Zhang, Hao / Kanwar, Yashpal S / Dai, Yingbo

    Cells

    2022  Volume 12, Issue 1

    Abstract: ... ...

    Abstract Myo
    MeSH term(s) Animals ; Mice ; Acute Kidney Injury/chemically induced ; Acute Kidney Injury/drug therapy ; Carrier Proteins ; Cisplatin/pharmacology ; Dietary Supplements ; Ferroptosis ; Inositol/metabolism ; Inositol/pharmacology
    Chemical Substances Carrier Proteins ; Cisplatin (Q20Q21Q62J) ; Inositol (4L6452S749)
    Language English
    Publishing date 2022-12-21
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12010016
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  7. Article ; Online: Modulation of gentamicin-induced acute kidney injury by myo-inositol oxygenase via the ROS/ALOX-12/12-HETE/GPR31 signaling pathway.

    Sharma, Isha / Liao, Yingjun / Zheng, Xiaoping / Kanwar, Yashpal S

    JCI insight

    2022  Volume 7, Issue 6

    Abstract: In this investigation, a potentially novel signaling pathway in gentamicin-induced acute kidney injury-worsened by overexpression of proximal tubular enzyme, myo-inositol oxygenase (MIOX)-was elucidated. WT, MIOX-transgenic (MIOX-Tg), and MIOX-KO mice ... ...

    Abstract In this investigation, a potentially novel signaling pathway in gentamicin-induced acute kidney injury-worsened by overexpression of proximal tubular enzyme, myo-inositol oxygenase (MIOX)-was elucidated. WT, MIOX-transgenic (MIOX-Tg), and MIOX-KO mice were used. Gentamicin was administered to induce tubular injury. MIOX-Tg mice had severe tubular lesions associated with increased serum creatinine and proteinuria. Lesions were relatively mild, with no rise in serum creatinine and no albuminuria in MIOX-KO mice. Transfection of HK-2 cells with MIOX-pcDNA led to increased gentamicin-induced reactive oxygen species (ROS). Marked increase of ROS-mediated lipid hydroperoxidation was noted in MIOX-Tg mice, as assessed by 4-HNE staining. This was associated with increased expression of arachidonate 12-lipoxygenase (ALOX-12) and generation of 12-hydroxyeicosatetraenoic acid (12-HETE). In addition, notable monocyte/macrophage influx, upregulation of NF-κB and inflammatory cytokines, and apoptosis was observed in MIOX-Tg mice. Treatment of cells with ALOX-12 siRNA abolished gentamicin-mediated induction of cytokines and 12-HETE generation. HETE-12 treatment promoted this effect, along with upregulation of various signaling kinases and activation of GPCR31. Similarly, treatment of cells or mice with the ALOX-12 inhibitor ML355 attenuated inflammatory response, kinase signaling cascade, and albuminuria. Collectively, these studies highlight a potentially novel mechanism (i.e., the ROS/ALOX-12/12-HETE/GPR31 signaling axis) relevant to gentamicin-induced nephrotoxicity modulated by MIOX.
    MeSH term(s) 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid/adverse effects ; Acute Kidney Injury/chemically induced ; Animals ; Creatinine ; Cytokines ; Gentamicins/toxicity ; Inositol Oxygenase/genetics ; Inositol Oxygenase/metabolism ; Mice ; Reactive Oxygen Species/metabolism ; Signal Transduction
    Chemical Substances Cytokines ; Gentamicins ; Reactive Oxygen Species ; 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid (59985-28-3) ; Creatinine (AYI8EX34EU) ; Inositol Oxygenase (EC 1.13.99.1)
    Language English
    Publishing date 2022-03-22
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.155487
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Modulation of gentamicin-induced acute kidney injury by myo-inositol oxygenase via the ROS/ALOX-12/12-HETE/GPR31 signaling pathway

    Isha Sharma / Yingjun Liao / Xiaoping Zheng / Yashpal S. Kanwar

    JCI Insight, Vol 7, Iss

    2022  Volume 6

    Abstract: In this investigation, a potentially novel signaling pathway in gentamicin-induced acute kidney injury—worsened by overexpression of proximal tubular enzyme, myo-inositol oxygenase (MIOX)—was elucidated. WT, MIOX-transgenic (MIOX-Tg), and MIOX-KO mice ... ...

    Abstract In this investigation, a potentially novel signaling pathway in gentamicin-induced acute kidney injury—worsened by overexpression of proximal tubular enzyme, myo-inositol oxygenase (MIOX)—was elucidated. WT, MIOX-transgenic (MIOX-Tg), and MIOX-KO mice were used. Gentamicin was administered to induce tubular injury. MIOX-Tg mice had severe tubular lesions associated with increased serum creatinine and proteinuria. Lesions were relatively mild, with no rise in serum creatinine and no albuminuria in MIOX-KO mice. Transfection of HK-2 cells with MIOX-pcDNA led to increased gentamicin-induced reactive oxygen species (ROS). Marked increase of ROS-mediated lipid hydroperoxidation was noted in MIOX-Tg mice, as assessed by 4-HNE staining. This was associated with increased expression of arachidonate 12-lipoxygenase (ALOX-12) and generation of 12-hydroxyeicosatetraenoic acid (12-HETE). In addition, notable monocyte/macrophage influx, upregulation of NF-κB and inflammatory cytokines, and apoptosis was observed in MIOX-Tg mice. Treatment of cells with ALOX-12 siRNA abolished gentamicin-mediated induction of cytokines and 12-HETE generation. HETE-12 treatment promoted this effect, along with upregulation of various signaling kinases and activation of GPCR31. Similarly, treatment of cells or mice with the ALOX-12 inhibitor ML355 attenuated inflammatory response, kinase signaling cascade, and albuminuria. Collectively, these studies highlight a potentially novel mechanism (i.e., the ROS/ALOX-12/12-HETE/GPR31 signaling axis) relevant to gentamicin-induced nephrotoxicity modulated by MIOX.
    Keywords Nephrology ; Medicine ; R
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Withdrawal:

    Sun, Lin / Dutta, Rajesh K / Xie, Ping / Kanwar, Yashpal S

    The Journal of biological chemistry

    2019  Volume 294, Issue 26, Page(s) 10380

    Language English
    Publishing date 2019-06-28
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W119.009586
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    Uc I Zs.108: Show issues Location:
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  10. Article: Modulation of Renal Injury by Variable Expression of Myo-Inositol Oxygenase (MIOX) via Perturbation in Metabolic Sensors.

    Sharma, Isha / Deng, Fei / Kanwar, Yashpal S

    Biomedicines

    2020  Volume 8, Issue 7

    Abstract: ... redox balance and subsequent tubular injury in the settings of obesity. Mechanism(s) for such adverse ...

    Abstract Obesity is associated with perturbations in cellular energy homeostasis and consequential renal injury leading to chronic renal disease (CKD). Myo-inositol oxygenase (MIOX), a tubular enzyme, alters redox balance and subsequent tubular injury in the settings of obesity. Mechanism(s) for such adverse changes remain enigmatic. Conceivably, MIOX accentuates renal injury via reducing expression/activity of metabolic sensors, which perturb mitochondrial dynamics and, if sustained, would ultimately contribute towards CKD. In this brief communication, we utilized MIOX-TG (Transgenic) and MIOX
    Language English
    Publishing date 2020-07-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines8070217
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