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https://www.readbyqxmd.com/read/28544853/microrna-34a-protect-myocardial-cells-against-ischemia-reperfusion-injury-through-inhibiting-autophagy-via-regulating-tnf%C3%AE-expression
#1
Haifeng Shao, Lili Yang, Li Wang, Bozan Tang, Jian Wang, Qiang Li
BACKGROUND: Ischemia/reperfusion (I/R) accompanying with the blood supply restored after myocardial infarction. Myocardial I/R injury relieves when autophagy decreased. MicroRNA-34a(miR-34a) regulate autophagy in renal I/R injury model. But whether it can affect cardiac I/R injury remains studying. This study investigated how miR-34a in protecting myocardial cells against I/R injury through inhibit autophagy via regulating tumor necrosis factor α (TNFα) . METHODS: Constructed the I/R model in vivo with Langendorff; treated Neonatal Rat cardiomyocyte to make H/R injury model in vitro with hypoxia/reoxygenation (H/R) method...
May 25, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/28539339/mif-2-d-dt-enhances-proximal-tubular-cell-regeneration-through-slpi-and-atf4-dependent-mechanisms
#2
Akinobu Ochi, Dong Chen, Wibke Schulte, Lin Leng, Nickolas Gilbert Moeckel, Marta Piecychna, Luisa Averdunk, Christian Stoppe, Richard Bucala, Gilbert W Moeckel
Macrophage migration inhibitory factor (MIF) is a cytokine with pleiotropic actions that is produced by several organs and cell types. Depending on the target cell and the inflammatory context, MIF can engage its two component receptor complex CD74 and CD44, and the chemokine receptors CXCR2/4. MIF is constitutively expressed in renal proximal tubular cells, stored in intracellular preformed pools and is released at a low rate. Recently a second MIF-like protein (i.e. MIF-2/D-DT) has been characterized in mammals...
May 24, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28536471/caffeic-acid-attenuates-diabetic-kidney-disease-via-modulation-of-autophagy-in-a-high-fat-diet-streptozotocin-induced-diabetic-rat
#3
Marwa Matboli, Sanaa Eissa, Doaa Ibrahim, Marwa G A Hegazy, Shalabia S Imam, Eman K Habib
The aim of this study is to evaluate the anti-diabetic nephropathy effect of Caffeic acid and to prove our hypothesis for its mechanism of action that it may occur by reactivation of autophagy pathway via suppression of autophagy regulatory miRNAs. In vivo, high-fat diet and streptozotocin-induced (HFD-STZ) diabetic rats were treated with Caffeic acid once per day for 12 weeks before and after development of diabetic nephropathy. Blood and urine biochemical parameters, autophagy transcripts and their epigenetic regulators together with renal tissue morphology were investigated...
May 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28513870/activation-of-the-nrf2-are-signaling-pathway-prevents-hyperphosphatemia-induced-vascular-calcification-by-inducing-autophagy-in-renal-vascular-smooth-muscle-cells
#4
Li Yao, Jian Wang, Bin-Yao Tian, Tian-Hua Xu, Zi-Tong Sheng
This study investigates the effect of nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway in vascular calcification (VC) via inducing Autophagy in renal vascular smooth muscle cells (VSMCs). VSMCs were assigned into six experimental groups: the normal control, high phosphorus, si-negative control (si-NC), Nrf2-siRNA, over-expressed Nrf2 and negative control (NC) groups. RT-PCR was applied to detect the mRNA expressions of the desired Nrf2-ARE signaling pathway-related genes (Nrf2, NQO-1, HO-1, γ-GCS)...
May 17, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28512641/podocyte-autophagy-a-potential-therapeutic-target-to-prevent-the-progression-of-diabetic-nephropathy
#5
REVIEW
Na Liu, Liuqing Xu, Yingfeng Shi, Shougang Zhuang
Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD), becomes a worldwide problem. Ultrastructural changes of the glomerular filtration barrier, especially the pathological changes of podocytes, lead to proteinuria in patients with diabetes. Podocytes are major components of glomerular filtration barrier, lining outside of the glomerular basement membrane (GBM) to maintain the permeability of the GBM. Autophagy is a high conserved cellular process in lysosomes including impaired protein, cell organelles, and other contents in the cytoplasm...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28505110/green-tea-polyphenols-mimicking-the-effects-of-dietary-restriction-ameliorate-high-fat-diet-induced-kidney-injury-via-regulating-autophagy-flux
#6
Xiao Xie, Weijie Yi, Piwei Zhang, Nannan Wu, Qiaoqiao Yan, Hui Yang, Chong Tian, Siyun Xiang, Miying Du, Eskedar Getachew Assefa, Xuezhi Zuo, Chenjiang Ying
Epidemiological and experimental studies reveal that Western dietary patterns contribute to chronic kidney disease, whereas dietary restriction (DR) or dietary polyphenols such as green tea polyphenols (GTPs) can ameliorate the progression of kidney injury. This study aimed to investigate the renal protective effects of GTPs and explore the underlying mechanisms. Sixty Wistar rats were randomly divided into 6 groups: standard diet (STD), DR, high-fat diet (HFD), and three diets plus 200 mg/kg(bw)/day GTPs, respectively...
May 14, 2017: Nutrients
https://www.readbyqxmd.com/read/28499867/glycine-nitronyl-nitroxide-conjugate-protects-human-umbilical-vein-endothelial-cells-against-hypoxia-reoxygenation-injury-via-multiple-mechanisms-and-ameliorates-hind-limb-ischemia-reperfusion-injury-in-rats
#7
Xiang Gao, Yue Bi, Kui Chi, Yang Liu, Tao Yuan, Xueyan Li, Wei Bi
Oxidative stress and inflammation play important roles in the pathogenesis of ischemia/reperfusion (I/R)-injury. The administration of antioxidants and anti-inflammatory agents has been applied to prevent I/R-injury for several decades. Of the numerous compounds administrated therapeutically in anti-oxidative stress, nitronyl nitroxide has gained increasing attention due to its continuous ability to scavenge active oxygen radicals. However, its effect is not ideal in clinical therapy. In previous study, we linked the anti-inflammatory amino acid glycine to nitronyl nitroxide and developed a novel glycine-nitronyl nitroxide (GNN) conjugate, which showed a synergetic protection against renal ischemia/reperfusion injury...
June 17, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28491859/autophagy-in-kidney-transplants-of-sirolimus-treated-recipients
#8
Sagar Bhayana, Arpita Baisantry, Thomas D Kraemer, Christoph Wrede, Jan Hegermann, Jan-Hinrich Bräsen, Clemens Bockmeyer, Jan Ulrich Becker, Matthias Ochs, Wilfried Gwinner, Hermann Haller, Anette Melk, Roland Schmitt
BACKGROUND: Mammalian target of rapamycin (mTOR) inhibitors are increasingly used as immunosuppressive agents in kidney transplantation. In the experimental setting it has been shown that mTOR inhibitors promote autophagy, but the concept that this might also occur in transplant patients has not been addressed. OBJECTIVES: This study was designed to investigate the association between mTOR inhibition and autophagy in renal transplants under routine clinical conditions...
March 2017: Journal of Nephropathology
https://www.readbyqxmd.com/read/28472786/roles-of-the-exogenous-h2s-mediated-sr-a-signaling-pathway-in-renal-ischemia-reperfusion-injury-in-regulating-endoplasmic-reticulum-stress-induced-autophagy-in-a-rat-model
#9
Qing Ling, Xiao Yu, Tao Wang, Shao-Gang Wang, Zhang-Qun Ye, Ji-Hong Liu
OBJECTIVE: This study aims to explore the effects of the exogenous hydrogen sulfide (H2S)-mediated scavenger receptor A (SR-A) signaling pathway on renal ischemia/reperfusion injury (IRI) by regulating endoplasmic reticulum (ER) stress-induced autophagy in rats. METHODS: A total of 48 normal Sprague-Dawley (SD) rats and SR-A knockout rats were selected and divided into six groups (n = 8): wild-type (WT) + sham, WT + ischemia-reperfusion (I/R), WT + I/R + NaHS, SR-A-/- + sham, SR-A-/- + I/R and SR-A-/- + I/R + NaHS...
May 4, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28466106/augmenter-of-liver-regeneration-regulates-autophagy-in-renal-ischemia-reperfusion-injury-via-the-ampk-mtor-pathway
#10
Tao Pu, Xiao-Hui Liao, Hang Sun, Hui Guo, Xiao Jiang, Jun-Bo Peng, Ling Zhang, Qi Liu
Autophagy may have protective effects in renal ischemia-reperfusion (I/R) injury, although the underlying mechanisms remain unclear. Augmenter of liver regeneration (ALR), a widely distributed multifunctional protein that is originally identified as a hepatic growth factor, may participate in the process of autophagy. To investigate the role of ALR in autophagy, ALR expression is knocked-down in human kidney 2 (HK-2) cells with short hairpin RNA lentivirals. Then, the level of autophagy is measured in the shRNA/ALR group and the shRNA/control group in an in vitro model of ischemia-reperfusion (I/R)...
May 2, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28465352/cystinosin-the-small-gtpase-rab11-and-the-rab7-effector-rilp-regulate-intracellular-trafficking-of-the-chaperone-mediated-autophagy-receptor-lamp2a
#11
Jinzhong Zhang, Jennifer L Johnson, Jing He, Gennaro Napolitano, Mahalakshmi Ramadass, Celine Rocca, William B Kiosses, Cecilia Bucci, Qisheng Xin, Evripidis Gavathiotis, Ana María Cuervo, Stephanie Cherqui, Sergio D Catz
The lysosomal storage disease cystinosis, caused by cystinosin-deficiency, is characterized by cell malfunction, tissue failure and progressive renal injury despite cystine-depletion therapies. Cystinosis is associated with defects in chaperone-mediated autophagy (CMA), but the molecular mechanisms are incompletely understood. Here, we show CMA substrate accumulation in cystinotic kidney proximal tubule cells. We also found mislocalization of the CMA lysosomal receptor LAMP2A, and impaired substrate translocation into the lysosome caused by defective CMA in cystinosis...
May 2, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28445931/high-glucose-induces-apoptosis-via-upregulation-of-bim-expression-in-proximal-tubule-epithelial-cells
#12
Xiao-Qian Zhang, Jian-Jun Dong, Tian Cai, Xue Shen, Xiao-Jun Zhou, Lin Liao
Diabetic nephropathy is the primary cause of end-stage renal disease. Apoptosis of tubule epithelial cells is a major feature of diabetic nephropathy. The mechanisms of high glucose (HG) induced apoptosis are not fully understood. Here we demonstrated that, HG induced apoptosis via upregulating the expression of proapoptotic Bcl-2 homology domain 3 (BH3)-only protein Bim protein, but not bring a significant change in the baseline level of autophagy in HK2 cells. The increase of Bim expression was caused by the ugregulation of transcription factors, FOXO1 and FOXO3a...
April 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28437467/mutant-uromodulin-expression-leads-to-altered-homeostasis-of-the-endoplasmic-reticulum-and-activates-the-unfolded-protein-response
#13
Céline Schaeffer, Stefania Merella, Elena Pasqualetto, Dejan Lazarevic, Luca Rampoldi
Uromodulin is the most abundant urinary protein in physiological conditions. It is exclusively produced by renal epithelial cells lining the thick ascending limb of Henle's loop (TAL) and it plays key roles in kidney function and disease. Mutations in UMOD, the gene encoding uromodulin, cause autosomal dominant tubulointerstitial kidney disease uromodulin-related (ADTKD-UMOD), characterised by hyperuricemia, gout and progressive loss of renal function. While the primary effect of UMOD mutations, retention in the endoplasmic reticulum (ER), is well established, its downstream effects are still largely unknown...
2017: PloS One
https://www.readbyqxmd.com/read/28428331/a-personalized-model-of-coq2-nephropathy-rescued-by-the-wild-type-coq2-allele-or-dietary-coenzyme-q10-supplementation
#14
Jun-Yi Zhu, Yulong Fu, Adam Richman, Zhanzheng Zhao, Patricio E Ray, Zhe Han
Clinical studies have identified patients with nephrotic syndrome caused by mutations in genes involved in the biosynthesis of coenzyme Q10 (CoQ10), a lipid component of the mitochondrial electron transport chain and an important antioxidant. However, the cellular mechanisms through which these mutations induce podocyte injury remain obscure. Here, we exploited the striking similarities between Drosophila nephrocytes and human podocytes to develop a Drosophila model of these renal diseases, and performed a systematic in vivo analysis assessing the role of CoQ10 pathway genes in renal function...
April 20, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/28424210/ucp2-attenuates-apoptosis-of-tubular-epithelial-cells-in-renal-ischemia-reperfusion-injury
#15
Yang Zhou, Ting Cai, Jing Xu, Lei Jiang, Jining Wu, Qi Sun, Ke Zen, Junwei Yang
Uncoupling protein 2 (UCP2) plays critical roles in energy metabolism and cell survival. Previous investigations showed that UCP2 regulated the production of extracellular matrix and renal fibrosis. However, little is known about UCP2 in acute kidney injury. Here, we used UCP2 knockout mice to investigate the role of UCP2 in AKI model generated by renal ischemia/reperfusion (I/R) injury. The UCP2 global knockout mice were born and growth normal without kidney histological abnormality or renal dysfunctions. As compared with littermates, deletion of UCP2 exacerbated I/R-induced AKI while increase of UCP2 by conjugated linoleic acid (CLA) attenuated I/R injury...
April 19, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28423497/drp1-dependent-mitophagy-protects-against-cisplatin-induced-apoptosis-of-renal-tubular-epithelial-cells-by-improving-mitochondrial-function
#16
Chuanyan Zhao, Zhuyun Chen, Jia Qi, Suyan Duan, Zhimin Huang, Chengning Zhang, Lin Wu, Ming Zeng, Bo Zhang, Ningning Wang, Huijuan Mao, Aihua Zhang, Changying Xing, Yanggang Yuan
Cisplatin chemotherapy often causes acute kidney injury (AKI) in cancer patients. There is increasing evidence that mitochondrial dysfunction plays an important role in cisplatin-induced nephrotoxicity. Degradation of damaged mitochondria is carried out by mitophagy. Although mitophagy is considered of particular importance in protecting against AKI, little is known of the precise role of mitophagy and its molecular mechanisms during cisplatin-induced nephrotoxicity. Also, evidence that activation of mitophagy improved mitochondrial function is lacking...
March 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28417340/preconditioning-of-primary-human-renal-proximal-tubular-epithelial-cells-without-tryptophan-increases-survival-under-hypoxia-by-inducing-autophagy
#17
Theodoros Eleftheriadis, Georgios Pissas, Maria Sounidaki, Nikolaos Antoniadis, Georgia Antoniadi, Vassilios Liakopoulos, Ioannis Stefanidis
PURPOSE: Hypoxia plays a significant role in the pathogenesis of acute kidney injury (AKI). Autophagy protects from AKI. Amino acid deprivation induces autophagy. The effect of L-tryptophan depletion on survival and autophagy in cultures of renal proximal tubular epithelial cells (RPTECs) under hypoxia was evaluated. METHODS: RPTECs were preconditioned in a medium containing or not tryptophan, following culture under hypoxia and treatment with or without the autophagy inhibitor chloroquine...
April 17, 2017: International Urology and Nephrology
https://www.readbyqxmd.com/read/28417246/mammalian-target-of-rapamycin-mtor-as-a-potential-therapeutic-target-in-various-diseases
#18
REVIEW
Avileen Kaur, Saurabh Sharma
Mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase that belongs to Phosphatidylinositol-3-kinase related kinase superfamily. The signaling pathways of mTOR are integrated through the protein complexes of mTORC1 and mTORC2. mTORC1 controls protein synthesis, cell growth, proliferation, autophagy, cell metabolism, and stress responses, whereas mTORC2 seems to regulate cell survival and polarity. Dysregulation of the mTOR pathway has been implicated in the pathophysiology of a number of disease conditions, including cancer, cardiovascular, neurodegenerative, and various renal diseases...
June 2017: Inflammopharmacology
https://www.readbyqxmd.com/read/28409163/pgc1%C3%AE-activators-mitigate-diabetic-tubulopathy-by-improving-mitochondrial-dynamics-and-quality-control
#19
So-Young Lee, Jun Mo Kang, Dong-Jin Kim, Seon Hwa Park, Hye Yun Jeong, Yu Ho Lee, Yang Gyun Kim, Dong Ho Yang, Sang Ho Lee
Purpose. In this study, we investigated the effect of PGC1α activators on mitochondrial fusion, fission, and autophagic quality control in renal tubular cells in a diabetic environment in vivo and in vitro. We also examined whether the upregulation of PGC1α attenuates diabetic tubulopathy by normalizing mitochondrial homeostasis. Methods. HKC8 cells were subjected to high-glucose conditions (30 mM D-glucose). Diabetes was induced with streptozotocin (STZ, 50 mg/kg i.p. for 5 days) in male C57/BL6J mice...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28408883/alisol-a-24-acetate-and-alisol-b-23-acetate-induced-autophagy-mediates-apoptosis-and-nephrotoxicity-in-human-renal-proximal-tubular-cells
#20
Chunfei Wang, Liang Feng, Liang Ma, Haifeng Chen, Xiaobin Tan, Xuefeng Hou, Jie Song, Li Cui, Dan Liu, Juan Chen, Nan Yang, Jing Wang, Ying Liu, Bingjie Zhao, Gang Wang, Yuanli Zhou, Xiaobin Jia
Two natural compounds alisol A 24-acetate (24A) and alisol B 23-acetate (23B) are abundant in Rhizoma alismatis. In the present study, we evaluated the induction of 24A and 23B on apoptosis and possible nephrotoxicity of human renal proximal tubular (HK-2) cells by activating autophagy and also explored its regulation on PI3K/Akt/mTOR signaling pathway. Presently, Clusterin, Kim-1, and TFF-3 were considered to be new bioindicators of nephrotoxicity. Interestingly, the protein expression and mRNA levels of Clusterin, Kim-1 and TFF-3 could be significantly increased by 23B and 24A in vivo and in vitro...
2017: Frontiers in Pharmacology
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