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Nephrology

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Methylation in pericytes after acute injury promotes chronic kidney disease
Yu-Hsiang Chou, … , Tzong-Shinn Chu, Shuei-Liong Lin
Yu-Hsiang Chou, … , Tzong-Shinn Chu, Shuei-Liong Lin
Published August 4, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI135773.
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Methylation in pericytes after acute injury promotes chronic kidney disease

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Abstract

The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury–induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.

Authors

Yu-Hsiang Chou, Szu-Yu Pan, Yu-Han Shao, Hong-Mou Shih, Shi-Yao Wei, Chun-Fu Lai, Wen-Chih Chiang, Claudia Schrimpf, Kai-Chien Yang, Liang-Chuan Lai, Yung-Ming Chen, Tzong-Shinn Chu, Shuei-Liong Lin

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Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression
Anqun Chen, … , Kyung Lee, John Cijiang He
Anqun Chen, … , Kyung Lee, John Cijiang He
Published July 7, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI140155.
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Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression

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Abstract

Utilizing the Nephrotic Syndrome Study Network Consortium and other publicly available transcriptomic datasets, we identified Retinoic acid receptor responder protein 1 (RARRES1) as a gene whose expression positively correlated with renal function decline in human glomerular disease. The glomerular expression of RARRES1, which is largely restricted to podocytes, increased in focal segmental glomerulosclerosis (FSGS) and diabetic kidney disease (DKD). Tumor necrosis factor-α (TNF-α) was a potent inducer of RARRES1 expression in cultured podocytes, and transcriptomic analysis showed the enrichment of cell death pathway genes with RARRES1 overexpression. The overexpression of RARRES1 indeed induced podocyte apoptosis in vitro. Notably, this effect was dependent on its cleavage in the extracellular domain, as the mutation of its cleavage site abolished the apoptotic effect. Mechanistically, the soluble RARRES1 is endocytosed and interacts with and inhibits RIO kinase 1 (RIOK1), resulting in p53 activation and podocyte apoptosis. In mice, podocyte-specific overexpression of RARRES1 resulted in marked glomerular injury and albuminuria, while the overexpression of RARRES1 cleavage mutant had no effect. Conversely, podocyte-specific knockdown of Rarres1 in mice ameliorated glomerular injury in the setting of Adriamycin-induced nephropathy. Together, our study demonstrates an important role and the mechanism of RARRES1 in podocyte injury in glomerular disease.

Authors

Anqun Chen, Ye Feng, Han Lai, Wenjun Ju, Zhengzhe Li, Yu Li, Andrew Wang, Quan Hong, Fang Zhong, Chengguo Wei, Jia Fu, Tian-Jun Guan, Bi-Cheng Liu, Matthias Kretzler, Kyung Lee, John Cijiang He

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Salt causes aging-associated hypertension via vascular Wnt5a under Klotho deficiency
Wakako Kawarazaki, … , Takeshi Marumo, Toshiro Fujita
Wakako Kawarazaki, … , Takeshi Marumo, Toshiro Fujita
Published June 29, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI134431.
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Salt causes aging-associated hypertension via vascular Wnt5a under Klotho deficiency

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Abstract

Aging is associated with a high prevalence of hypertension due to elevated susceptibility of BP to dietary salt, but its mechanism is unknown. Serum levels of Klotho, an anti-aging factor, decline with age. We found that high salt (HS) increased BP in aged mice and young heterozygous Klotho-knockout mice and was associated with increased vascular expression of Wnt5a and p-MYPT1, which indicate RhoA activity. Not only the Wnt inhibitor LGK974 and the Wnt5a antagonist Box5 but Klotho supplementation inhibits HS-induced BP elevation, similarly to the Rho kinase inhibitor fasudil, associated with reduced p-MYPT1 expression in both groups of mice. In cultured vascular smooth muscle cells, Wnt5a and angiotensin II (Ang II) increased p-MYPT1 expression but knockdown of Wnt5a with siRNA abolished Ang II–induced upregulation of p-MYPT1, indicating that Wnt5a is indispensable for Ang II–induced Rho/ROCK activation. Notably, Klotho inhibited Wnt5a- and Ang II–induced upregulation of p-MYPT1. Consistently, Klotho supplementation ameliorated HS-induced augmentation of reduced renal blood flow (RBF) response to intra-arterial infusion of Ang II and the thromboxane A2 analog U46619, which activated RhoA in both groups of mice and were associated with the inhibition of BP elevation, suggesting that abnormal response of RBF to Ang II contributes to HS-induced BP elevation. Thus, Klotho deficiency underlies aging-associated salt-sensitive hypertension through vascular non-canonical Wnt5a/RhoA activation.

Authors

Wakako Kawarazaki, Risuke Mizuno, Mitsuhiro Nishimoto, Nobuhiro Ayuzawa, Daigoro Hirohama, Kohei Ueda, Fumiko Kawakami-Mori, Shigeyoshi Oba, Takeshi Marumo, Toshiro Fujita

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Pro-inflammatory P2Y14 receptor inhibition protects against ischemic acute kidney injury in mice
Maria Agustina Battistone, … , Dennis Brown, Sylvie Breton
Maria Agustina Battistone, … , Dennis Brown, Sylvie Breton
Published April 14, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI134791.
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Pro-inflammatory P2Y14 receptor inhibition protects against ischemic acute kidney injury in mice

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Abstract

Ischemic acute kidney injury (AKI), a complication that frequently occurs in hospital settings, is often associated with hemodynamic compromise, sepsis, cardiac surgery or exposure to nephrotoxicants. Here, using a murine renal ischemia-reperfusion injury (IRI) model we show that intercalated cells (ICs) rapidly adopted a pro-inflammatory phenotype post-IRI. During the early phase of AKI, we demonstrate that either blocking the pro-inflammatory P2Y14 receptor located on the apical membrane of ICs, or ablation of the gene encoding the P2Y14 receptor in ICs: 1) inhibited IRI-induced chemokine expression increase in ICs; 2) reduced neutrophil and monocyte renal infiltration; 3) reduced the extent of kidney dysfunction; and 4) attenuated proximal tubule (PT) damage. These observations indicate that the P2Y14 receptor participates in the very first inflammatory steps associated with ischemic AKI. In addition, we show that the concentration of the P2Y14 receptor ligand, uridine diphosphate-glucose (UDP-Glc), was higher in urine samples from intensive care unit patients who developed AKI compared to patients without AKI. In particular, we observed a strong correlation between UDP-Glc concentration and the development of AKI in cardiac surgery patients. Our study identifies the UDP-Glc/P2Y14 receptor axis as a potential target for the prevention and/or attenuation of ischemic-AKI.

Authors

Maria Agustina Battistone, Alexandra C. Mendelsohn, Raul German Spallanzani, Andrew S. Allegretti, Rachel N. Liberman, Juliana Sesma, Sahir Kalim, Susan M. Wall, Joseph V. Bonventre, Eduardo R. Lazarowski, Dennis Brown, Sylvie Breton

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Claudin-2 deficiency associates with hypercalciuria in mice and human kidney stone disease
Joshua N. Curry, … , Koichi Matsuda, Alan S.L. Yu
Joshua N. Curry, … , Koichi Matsuda, Alan S.L. Yu
Published March 9, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI127750.
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Claudin-2 deficiency associates with hypercalciuria in mice and human kidney stone disease

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Abstract

The major risk factor for kidney stone disease is idiopathic hypercalciuria. Recent evidence implicates a role for defective calcium reabsorption in the renal proximal tubule. We hypothesized that claudin-2, a paracellular cation channel protein, mediates proximal tubule calcium reabsorption. We found that claudin-2–null mice have hypercalciuria due to a primary defect in renal tubule calcium transport and papillary nephrocalcinosis that resembles the intratubular plugs in kidney stone formers. Our findings suggest that a proximal tubule defect in calcium reabsorption predisposes to papillary calcification, providing support for the vas washdown hypothesis. Claudin-2–null mice were also found to have increased net intestinal calcium absorption, but reduced paracellular calcium permeability in the colon, suggesting that this was due to reduced intestinal calcium secretion. Common genetic variants in the claudin-2 gene were associated with decreased tissue expression of claudin-2 and increased risk of kidney stones in 2 large population-based studies. Finally, we describe a family in which males with a rare missense variant in claudin-2 have marked hypercalciuria and kidney stone disease. Our findings indicate that claudin-2 is a key regulator of calcium excretion and a potential target for therapies to prevent kidney stones.

Authors

Joshua N. Curry, Matthew Saurette, Masomeh Askari, Lei Pei, Michael B. Filla, Megan R. Beggs, Peter S.N. Rowe, Timothy Fields, Andre J. Sommer, Chizu Tanikawa, Yoichiro Kamatani, Andrew P. Evan, Mehdi Totonchi, R. Todd Alexander, Koichi Matsuda, Alan S.L. Yu

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Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney
Petra Simic, … , Marc N. Wein, Eugene P. Rhee
Petra Simic, … , Marc N. Wein, Eugene P. Rhee
Published February 17, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI131190.
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Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney

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Abstract

Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that controls blood phosphate levels by increasing renal phosphate excretion and reducing 1,25-dihydroxyvitamin D3 [1,25(OH)2D] production. Disorders of FGF23 homeostasis are associated with significant morbidity and mortality, but a fundamental understanding of what regulates FGF23 production is lacking. Because the kidney is the major end organ of FGF23 action, we hypothesized that it releases a factor that regulates FGF23 synthesis. Using aptamer-based proteomics and liquid chromatography–mass spectrometry–based (LC-MS–based) metabolomics, we profiled more than 1600 molecules in renal venous plasma obtained from human subjects. Renal vein glycerol-3-phosphate (G-3-P) had the strongest correlation with circulating FGF23. In mice, exogenous G-3-P stimulated bone and bone marrow FGF23 production through local G-3-P acyltransferase–mediated (GPAT-mediated) lysophosphatidic acid (LPA) synthesis. Further, the stimulatory effect of G-3-P and LPA on FGF23 required LPA receptor 1 (LPAR1). Acute kidney injury (AKI), which increases FGF23 levels, rapidly increased circulating G-3-P in humans and mice, and the effect of AKI on FGF23 was abrogated by GPAT inhibition or Lpar1 deletion. Together, our findings establish a role for kidney-derived G-3-P in mineral metabolism and outline potential targets to modulate FGF23 production during kidney injury.

Authors

Petra Simic, Wondong Kim, Wen Zhou, Kerry A. Pierce, Wenhan Chang, David B. Sykes, Najihah B. Aziz, Sammy Elmariah, Debby Ngo, Paola Divieti Pajevic, Nicolas Govea, Bryan R. Kestenbaum, Ian H. de Boer, Zhiqiang Cheng, Marta Christov, Jerold Chun, David E. Leaf, Sushrut S. Waikar, Andrew M. Tager, Robert E. Gerszten, Ravi I. Thadhani, Clary B. Clish, Harald Jüppner, Marc N. Wein, Eugene P. Rhee

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FOXM1 drives proximal tubule proliferation during repair from acute ischemic kidney injury
Monica Chang-Panesso, … , Akio Kobayashi, Benjamin D. Humphreys
Monica Chang-Panesso, … , Akio Kobayashi, Benjamin D. Humphreys
Published November 11, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI125519.
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FOXM1 drives proximal tubule proliferation during repair from acute ischemic kidney injury

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The proximal tubule has a remarkable capacity for repair after acute injury, but the cellular lineage and molecular mechanisms underlying this repair response are incompletely understood. Here, we developed a Kim1-GFPCreERt2 knockin mouse line (Kim1-GCE) in order to perform genetic lineage tracing of dedifferentiated cells while measuring the cellular transcriptome of proximal tubule during repair. Acutely injured genetically labeled clones coexpressed KIM1, VIMENTIN, SOX9, and KI67, indicating a dedifferentiated and proliferative state. Clonal analysis revealed clonal expansion of Kim1+ cells, indicating that acutely injured, dedifferentiated proximal tubule cells, rather than fixed tubular progenitor cells, account for repair. Translational profiling during injury and repair revealed signatures of both successful and unsuccessful maladaptive repair. The transcription factor Foxm1 was induced early in injury, was required for epithelial proliferation in vitro, and was dependent on epidermal growth factor receptor (EGFR) stimulation. In conclusion, dedifferentiated proximal tubule cells effect proximal tubule repair, and we reveal an EGFR/FOXM1-dependent signaling pathway that drives proliferative repair after injury.

Authors

Monica Chang-Panesso, Farid F. Kadyrov, Matthew Lalli, Haojia Wu, Shiyo Ikeda, Eirini Kefaloyianni, Mai M. Abdelmageed, Andreas Herrlich, Akio Kobayashi, Benjamin D. Humphreys

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Human C-terminal CUBN variants associate with chronic proteinuria and normal renal function
Mathilda Bedin, … , Corinne Antignac, Matias Simons
Mathilda Bedin, … , Corinne Antignac, Matias Simons
Published October 15, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI129937.
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Human C-terminal CUBN variants associate with chronic proteinuria and normal renal function

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Abstract

Background: Proteinuria is considered as an unfavorable clinical condition that accelerates renal and cardiovascular disease. However, it is not clear if all forms of proteinuria are damaging. Mutations in CUBN cause Imerslund-Gräsbeck syndrome (IGS) featured by intestinal malabsorption of vitamin B12 and in some cases proteinuria. CUBN encodes for cubilin, an intestinal and proximal tubular uptake receptor containing 27 CUB domains for ligand binding. Methods: We used next-generation sequencing for renal disease genes to genotype cohorts of patients with suspected hereditary renal disease and chronic proteinuria. CUBN variants were analyzed using bioinformatics, structural modeling and epidemiological methods. Results: We identified 39 patients, in whom biallelic pathogenic variants in the CUBN gene are associated with chronic isolated proteinuria with childhood onset. Since the proteinuria displayed a high proportion of albuminuria, glomerular diseases such as steroid-resistant nephrotic syndrome or Alport syndrome were often the primary clinical diagnosis, motivating renal biopsies and proteinuria-lowering treatments. Yet, renal function was normal in all cases. By contrast, we did not find any biallelic pathogenic CUBN variants in patients with reduced renal function or focal segmental glomerulosclerosis. Unlike the more N-terminal IGS mutations, 37 out of the 41 proteinuria-associated CUBN variants led to modifications or truncations after the vitamin B12-binding domain. Finally, we show that four C-terminal CUBN variants are associated with albuminuria and moderately increased GFR in meta-analyses of large population-based cohorts. Conclusions: Collectively, our data suggest an important role for the C-terminal half of cubilin in renal albumin reabsorption. Albuminuria due to reduced cubilin function could be an unexpectedly common benign condition in humans that may not require any proteinuria-lowering treatment or renal biopsies.

Authors

Mathilda Bedin, Olivia Boyer, Aude Servais, Yong Li, Laure Villoing-Gaudé, Marie-Josephe Tête, Alexandra Cambier, Julien Hogan, Veronique Baudouin, Saoussen Krid, Albert Bensman, Florie Lammens, Ferielle Louillet, Bruno Ranchin, Cecile Vigneau, Iseline Bouteau, Corinne Isnard-Bagnis, Christoph J. Mache, Tobias Schäfer, Lars Pape, Markus Gödel, Tobias B. Huber, Marcus Benz, Günter Klaus, Matthias Hansen, Kay Latta, Olivier Gribouval, Vincent Morinière, Carole Tournant, Maik Grohmann, Elisa Kuhn, Timo Wagner, Christine Bole-Feysot, Fabienne Jabot-Hanin, Patrick Nitschké, Tarunveer S. Ahluwalia, Anna Köttgen, Christian Brix Folsted Andersen, Carsten Bergmann, Corinne Antignac, Matias Simons

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Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses
Seiji Kishi, … , Ryuji Morizane, Joseph V. Bonventre
Seiji Kishi, … , Ryuji Morizane, Joseph V. Bonventre
Published October 7, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI122313.
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Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses

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Abstract

Maladaptive proximal tubule (PT) repair has been implicated in kidney fibrosis through induction of cell-cycle arrest at G2/M. We explored the relative importance of the PT DNA damage response (DDR) in kidney fibrosis by genetically inactivating ataxia telangiectasia and Rad3-related (ATR), which is a sensor and upstream initiator of the DDR. In human chronic kidney disease, ATR expression inversely correlates with DNA damage. ATR was upregulated in approximately 70% of Lotus tetragonolobus lectin–positive (LTL+) PT cells in cisplatin-exposed human kidney organoids. Inhibition of ATR resulted in greater PT cell injury in organoids and cultured PT cells. PT-specific Atr-knockout (ATRRPTC–/–) mice exhibited greater kidney function impairment, DNA damage, and fibrosis than did WT mice in response to kidney injury induced by either cisplatin, bilateral ischemia-reperfusion, or unilateral ureteral obstruction. ATRRPTC–/– mice had more cells in the G2/M phase after injury than did WT mice after similar treatments. In conclusion, PT ATR activation is a key component of the DDR, which confers a protective effect mitigating the maladaptive repair and consequent fibrosis that follow kidney injury.

Authors

Seiji Kishi, Craig R. Brooks, Kensei Taguchi, Takaharu Ichimura, Yutaro Mori, Akinwande Akinfolarin, Navin Gupta, Pierre Galichon, Bertha C. Elias, Tomohisa Suzuki, Qian Wang, Leslie Gewin, Ryuji Morizane, Joseph V. Bonventre

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Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule
Fei Deng, … , Ming Yang, Yashpal S. Kanwar
Fei Deng, … , Ming Yang, Yashpal S. Kanwar
Published August 22, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI129903.
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Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule

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Abstract

Overexpression of myo-inositol oxygenase (MIOX), a proximal tubular enzyme, exacerbates cellular redox injury in acute kidney injury (AKI). Ferroptosis, a newly coined term associated with lipid hydroperoxidation, plays a critical role in the pathogenesis of AKI. Whether or not MIOX exacerbates tubular damage by accelerating ferroptosis in Cisplatin-induced AKI remains elusive. Cisplatin-treated HK-2 cells exhibited notable cell death, which was reduced by ferroptosis inhibitors. Also, alterations in various ferroptosis metabolic sensors, including lipid hydroperoxidation, glutathione peroxidase 4 (GPX4) activity, NADPH and reduced glutathione (GSH) levels, and ferritinophagy, were observed. These perturbations were accentuated by MIOX overexpression, while ameliorated by MIOX knockdown. Likewise, Cisplatin-treated CD1 mice exhibited tubular damage and derangement of renal physiological parameters, which was alleviated by Ferrostatin-1 (Fer-1), a ferroptosis inhibitor. To investigate the relevance of MIOX to ferroptosis, Wild-type (WT) mice, MIOX-overexpressing transgenic (MIOX-TG) mice and MIOX knockout (MIOX-KO) mice were subjected to Cisplatin treatment. In comparison to Cisplatin-treated WT mice, Cisplatin-treated MIOX-TG mice had more severe renal pathological changes and perturbations in ferroptosis metabolic sensors, which were minimal in Cisplatin-treated MIOX-KO mice. In conclusion, these findings indicate that ferroptosis, an integral process in the pathogenesis of Cisplatin-induced AKI, is modulated by the expression profile of MIOX.

Authors

Fei Deng, Isha Sharma, Yingbo Dai, Ming Yang, Yashpal S. Kanwar

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Local TNF mediates free cholesterol–dependent podocyte injury
In this episode, Alessia Fornoni reveals that TNF promotes free cholesterol–dependent podocyte apoptosis via an NFATc1/ ABCA1-dependent mechanism.
Published August 2, 2016
Author's TakeNephrology

Anti-THSD7A is a bona fide culprit in membranous nephropathy
Nicola M. Tomas, Elion Hoxha, and colleagues provide evidence that anti-THSD7A antibodies promote the development of membranous nephropathy...
Published May 23, 2016
Scientific Show StopperNephrology

Identifying sporadic focal segmental glomerulosclerosis-associated genes
Haiyang Yu, Mykyta Artomov, Sebastian Brähler and colleagues demonstrate the genetic contribution to the development of focal segmental glomerulosclerosis...
Published February 22, 2016
Scientific Show StopperNephrology

DNA replication stress linked to ciliopathies
Gisela Slaats and colleagues reveal that ciliopathy syndrome-associated mutations in CEP290 result in replication errors and DNA damage…
Published August 24, 2015
Scientific Show StopperNephrology

Nephrotic syndrome-associated mutations
Heon Yung Gee, Fujian Zhang, and colleagues reveal that mutations in KANK family genes underlie podocyte dysfunction and are associated with nephrotic syndrome…
Published May 11, 2015
Scientific Show StopperNephrology

Podocyte macropinocytosis
Jun-Jae Chung, Tobias B. Huber, Markus Gödel, and colleagues show that albumin-bound free fatty acids increase fluid-phase uptake in podocytes…
Published April 27, 2015
Scientific Show StopperNephrology

A network of diuretic resistance
Richard Grimm and colleagues use a systems biology approach to uncover mechanisms of renal compensation that lead to diuretic resistance…
Published April 20, 2015
Scientific Show StopperNephrology

KIM-1 protects the kidney after injury
Li Yang, Craig Brooks, and colleagues at Harvard Medical School demonstrate that KIM-1-mediated phagocytosis of apoptotic cells dampens inflammatory responses after kidney injury.. .
Published March 9, 2015
Scientific Show StopperNephrology

Protection against acute kidney injury
Marina Morigi and colleagues demonstrate that sirtuin 3 expression improves survival in a murine model of acute kidney injury...
Published January 20, 2015
Scientific Show StopperNephrology

Helping polycysin-1 reach the surface
Vladimir Gainullin and colleagues reveal that polycystin-2 is required for maturation and surface localization of polycystin-1…
Published January 9, 2015
Scientific Show StopperNephrology
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