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  1. 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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  2. 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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  3. 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
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  4. 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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  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: 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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  7. 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: 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 ... ...

    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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  8. Article ; Online: AL Amyloidosis Presenting With Crescentic Glomerulonephritis.

    Wang, Ann A / Kanwar, Yashpal S / Aggarwal, Vikram / Srivastava, Anand

    Kidney medicine

    2021  Volume 3, Issue 4, Page(s) 644–648

    Abstract: Kidney amyloidosis typically presents with nephrotic-range proteinuria. Rare cases of crescentic glomerulonephritis have been reported in patients with kidney amyloidosis but most cases were in the setting of patients with AA amyloidosis from long- ... ...

    Abstract Kidney amyloidosis typically presents with nephrotic-range proteinuria. Rare cases of crescentic glomerulonephritis have been reported in patients with kidney amyloidosis but most cases were in the setting of patients with AA amyloidosis from long-standing inflammation and malignancy. We present a case of a previously healthy man in his 70s who was admitted with severe acute kidney injury, nephrotic-range proteinuria, and nephritic urinary sediment. Initial serologic testing for causes of rapidly progressive glomerulonephritis were negative. Kidney biopsy demonstrated the presence of active cellular and fibrocellular crescents with Congo red-positive staining in glomeruli and microvasculature on light microscopy and amyloid fibrils in glomerular basement membrane on electron microscopy. Urinary protein electrophoresis revealed monoclonal λ light chains, leading to a diagnosis of kidney AL amyloidosis, which was confirmed with bone marrow biopsy. Our case illustrates that AL amyloidosis can present with findings suspicious for rapidly progressive glomerulonephritis and crescent formation on kidney biopsy specimens.
    Language English
    Publishing date 2021-04-20
    Publishing country United States
    Document type Case Reports
    ISSN 2590-0595
    ISSN (online) 2590-0595
    DOI 10.1016/j.xkme.2021.02.009
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  9. Article: New Pandemic: Obesity and Associated Nephropathy.

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

    Frontiers in medicine

    2021  Volume 8, Page(s) 673556

    Abstract: Incidence of obesity related renal disorders have increased 10-folds in recent years. One of the consequences of obesity is an increased glomerular filtration rate (GFR) that leads to the enlargement of the renal glomerulus, i.e., glomerulomegaly. This ... ...

    Abstract Incidence of obesity related renal disorders have increased 10-folds in recent years. One of the consequences of obesity is an increased glomerular filtration rate (GFR) that leads to the enlargement of the renal glomerulus, i.e., glomerulomegaly. This heightened hyper-filtration in the setting of type 2 diabetes irreparably damages the kidney and leads to progression of end stage renal disease (ESRD). The patients suffering from type 2 diabetes have progressive proteinuria, and eventually one third of them develop chronic kidney disease (CKD) and ESRD. For ameliorating the progression of CKD, inhibitors of renin angiotensin aldosterone system (RAAS) seemed to be effective, but on a short-term basis only. Long term and stable treatment strategies like weight loss via restricted or hypo-caloric diet or bariatric surgery have yielded better promising results in terms of amelioration of proteinuria and maintenance of normal GFR. Body mass index (BMI) is considered as a traditional marker for the onset of obesity, but apparently, it is not a reliable indicator, and thus there is a need for more precise evaluation of regional fat distribution and amount of muscle mass. With respect to the pathogenesis, recent investigations have suggested perturbation in fatty acid and cholesterol metabolism as the critical mediators in ectopic renal lipid accumulation associated with inflammation, increased generation of ROS, RAAS activation and consequential tubulo-interstitial injury. This review summarizes the renewed approaches for the obesity assessment and evaluation of the pathogenesis of CKD, altered renal hemodynamics and potential therapeutic targets.
    Language English
    Publishing date 2021-06-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2021.673556
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  10. Article ; Online: Aging and hemoglobin-induced acute kidney injury.

    Kanwar, Yashpal S

    American journal of physiology. Renal physiology

    2013  Volume 304, Issue 9, Page(s) F1167–8

    MeSH term(s) Acute Kidney Injury/chemically induced ; Aging/physiology ; Animals ; Female ; Hemeproteins/adverse effects ; Hemoglobins/adverse effects ; Kidney/physiopathology ; Kidney Tubular Necrosis, Acute/chemically induced ; Male
    Chemical Substances Hemeproteins ; Hemoglobins
    Language English
    Publishing date 2013-01-30
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00032.2013
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