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Fibrosis renal

Xiangcheng Xiao, Qiongjing Yuan, Yusa Chen, Zhihua Huang, Xi Fang, Haixia Zhang, Ling Peng, Ping Xiao
Although long noncoding RNA (LncRNA) are important players in the initiation and progression of many pathological processes, the role of LncRNAENST00000453774.1 (LncRNA 74.1) in renal fibrosis still remains unclear. Lentivirus mediated LncRNA 74.1 overexpressing HK2 cells and overexpression mice models were constructed. HK2 cells induced by transforming growth factor-β (TGF-β) in vitro, and the mice UUO model in vivo were used to simulate renal fibrosis. The expression of LncRNA 74.1 was significantly downregulated in the TGF-β-induced HK-2 cell fibrosis and clinical renal fibrosis specimens...
October 14, 2018: Journal of Cellular Physiology
S Sekito, K Nishikawa, S Masui, Y Hasegawa, H Kanda, K Arima, Y Sugimura
BACKGROUND: The frequency of renal transplants from elderly living donors has increased because of a shortage of donors. However, the results of renal transplantation using aged kidney grafts have yet to be determined conclusively. METHODS: We evaluated 45 patients who underwent living donor kidney transplantation at our institution. The patients were categorized according to donor age at the time of the transplant: ≥ 60 years (elderly donor group, n = 21) and <60 years (young donor group, n = 24)...
October 2018: Transplantation Proceedings
Iván Tavera Busso, Ana Carolina Mateos, Luis Isaías Juncos, Norma Canals, Hebe Alejandra Carreras
According to the WHO, about 3 million people die each year due to ambient air pollution. Most of the in vivo studies on the PM2.5 effects have been done on respiratory and cardiovascular tissues. However, little is known about the effects on the tissues involved on xenobiotic removal, such as kidneys. In the present study we assess the harmful effects of sub-chronic exposure to PM2.5 on the kidney, by investigating histologic and serum alterations in healthy and hypertensive rat models. Mean PM2.5 concentrations during exposures were slightly above the daily WHO standard...
October 10, 2018: Environment International
Shaoqun Shu, Jiefu Zhu, Zhiwen Liu, Chengyuan Tang, Juan Cai, Zheng Dong
BACKGROUND: Acute kidney injury (AKI) may lead to the development of chronic kidney disease (CKD), i.e. AKI-CKD transition, but the underlying mechanism remains largely unclear. Endoplasmic reticulum (ER) stress is characterized by the accumulation of unfolded or misfolded proteins in ER resulting in a cellular stress response. The role of ER stress in AKI-CKD transition remains unknown. METHODS: In this study, we examined ER stress in the mouse model of AKI-CKD transition after unilateral renal ischemia-reperfusion injury (uIR)...
October 9, 2018: EBioMedicine
Beverly Giam, Po-Yin Chu, Sanjaya Kuruppu, A Ian Smith, Duncan Horlock, Aishwarya Murali, Helen Kiriazis, Xiao-Jun Du, David M Kaye, Niwanthi W Rajapakse
What is the central question of this study? To determine the reno-protective effects of serelaxin in the setting of chronic heart failure. What are the main findings and its importance? Our data indicate that serelaxin can reduce renal fibrosis and inflammation in experimental heart failure. Currently, there are no effective treatments to rescue renal function in heart failure patients and our data suggest that serelaxin may have the potential to reduce renal fibrosis and inflammation in heart failure. ABSTRACT: Serelaxin has been demonstrated to attenuate renal fibrosis and inflammation in cardiorenal disease...
October 12, 2018: Experimental Physiology
Shahin Shadnia, Alireza Ebadollahi-Natanzi, Saeid Ahmadzadeh, Somayyeh Karami-Mohajeri, Yaghoub Pourshojaei, Hamid Reza Rahimi
Paraquat (PQ) poisoning is principally reported in developing countries. However, most fatalities occur elsewhere due to the induction of multi-organ failure. PQ poisoning can hardly be managed by clinical practice, and no specific antidote has come into existence yet. Here three cases, including 17-, 20-, and 23-year-old men, who were poisoned with PQ, have been reported. Furthermore, the literature regarding biological mechanisms, clinical manifestation, and treatment of PQ-induced toxicity was reviewed. Patients who, either intentionally or accidentally, ingested PQ earlier were initially found to be stable at the emergency department (ED)...
September 1, 2018: Toxicology Research
Juan Kong, Li Han, Han Su, Yihan Hu, Xueshi Huang, Yan Lou
BACKGROUND/AIMS: Nephropathy related with renin can be alleviated with ACE-inhibitors or AT1R blockers, whereas they might be ineffective after long-term administration because of a feedback production of enhanced renin. Therefore, it is urgent to develop a new category of anti-nephropathy medicine directly targeting renin. Riligustilide (C20), originally isolated from the Chinese herb Ligusticumporteri, a rhizome, was confirmed effective against many diseases. METHODS: The therapeutic effect of C20 on renal injury and its underlying mechanism were investigated in three different nephrotic models, which were spontaneously hypertension rats (SHR) model, diabetic nephropathy in BTBR ob/ob mice model and 5/6-nephrectomized (5/6NX) rats model...
October 11, 2018: Cellular Physiology and Biochemistry
Xiaoyang Wang, Guangjie Wang, Xiaoxue Zhang, Yanna Dou, Yijun Dong, Dong Liu, Jing Xiao, Zhanzheng Zhao
MiR-182-5p suppresses expression of Foxo1 that is a protective factor in renal disorders and is up-regulated in systemic lupus erythematosus patients. Thus, we hypothesized that dys-function of miR-182-5p/Foxo1 axis contributed to development of lupus nephritis (LN). Firstly, we investigated the expressions of miR-182-5p and Foxo1 in LN patients and during growth of LN MRL/lpr mice. Then we subjected MRL/lpr mice to the injection of miR-182-5p antagomirs and assessed the effect of miR-182-5p inhibition on renal structure and function...
October 8, 2018: Experimental Cell Research
Peng Wang, Man-Li Luo, Erwei Song, Zhanmei Zhou, Tongtong Ma, Jun Wang, Nan Jia, Guobao Wang, Sheng Nie, Youhua Liu, FanFan Hou
Transforming growth factor-β (TGF-β) is a well-established central mediator of renal fibrosis, a common outcome of almost all progressive chronic kidney diseases. Here, we identified a poorly conserved and kidney-enriched long noncoding RNA in TGF-β1-stimulated human tubular epithelial cells and fibrotic kidneys, which we termed TGF-β/Smad3-interacting long noncoding RNA ( lnc-TSI ). Lnc-TSI was transcriptionally regulated by Smad3 and specifically inhibited TGF-β-induced Smad3 phosphorylation and downstream profibrotic gene expression...
October 10, 2018: Science Translational Medicine
Qihan Luo, Zhaowei Cai, Jue Tu, Yun Ling, Dejun Wang, Yueqin Cai
BACKGROUND: Smilax glabra Roxb, a traditional Chinese herb, has been widely used in folk medicine. The current study was performed to investigate the protective effect of S. glabra Roxb extract, pure total flavonoids from Smilax glabra Roxb (PTFS), on renal interstitial fibrosis (RIF) and its underlying mechanism. METHODS: First, a surgical model of unilateral ureteral obstruction was established in rats to induce RIF. Then, rats were grouped and treated with PTFS at different concentration...
October 10, 2018: Journal of Cellular Biochemistry
Chang Seong Kim, In Jin Kim, Joon Seok Choi, Eun Hui Bae, Seong Kwon Ma, Soo Wan Kim
BACKGROUND INFORMATION: Tubulointerstitial fibrosis is the end-point of chronic kidney diseases. Tamoxifen, a selective estrogen receptor (ER) modulator, attenuates renal fibrosis, by regulating the transforming growth factor (TGF)-β/Smad signaling. Src and phosphoinositide 3-kinase (PI3K)/Akt pathways play critical roles in the pathogenesis of renal fibrosis. However, the activation of the non-canonical TGF-β signaling in renal fibrosis after treatment with tamoxifen remains unclear...
October 10, 2018: Biology of the Cell
Hong Ding, Ying Zhou, Haihua Huang
Hypertensive nephropathy, clinically characterized by progressive renal fibrosis and inflammation, is a severe complication of hypertension. The objectives of this study were to investigate the roles of miR-101a in relieving Angiotensin II (Ang II)-mediated hypertensive nephropathy and uncover the possible underlying mechanisms. Hypertensive mouse model was established via continuous 28-day AngII infusion. Systolic blood pressure (SBP), ratio of urine albumin to creatinine, blood urea nitrogen (BUN), serum creatinine (Scr) and glomerular filtration rate (GFR) were evaluated...
October 10, 2018: Clinical and Experimental Pharmacology & Physiology
Maria Fernanda Soares, Vera Genitsch, Aron Chakera, Andrew Smith, Clare MacEwen, Shubha S Bellur, Ian S D Roberts
AIMS: The Oxford Classification E score (endocapillary hypercellularity) predicts renal functional decline in IgA nephropathy (IgAN) patients free from steroid/immunosuppressive (IS) therapy, but is poorly reproducible. We hypothesise that endocapillary hypercellularity reflects glomerular inflammation and that the presence of CD68-positive cells is a more robust marker of E score. METHODS AND RESULTS: CD68 positive cells were quantified in glomeruli and tubulointerstitium in biopsies from 118 IgAN patients, and cell counts were correlated with the criteria of the Oxford Classification, assigned on PAS-stained serial sections...
October 10, 2018: Histopathology
Jiming Yin, Yangjia Wang, Jing Chang, Bin Li, Jia Zhang, Yu Liu, Song Lai, Ying Jiang, Huihua Li, Xiangjun Zeng
The epithelial-mesenchymal transition (EMT) of podocytes had been reported to be involved in the glomerular fibrosis in diabetic kidney diseases, which was regulated by TGFβ and NFκB pathways. And apelin, an adipokine which is upregulated in diabetic kidney diseases, was reported to be negatively correlated to TGFβ in polycystic kidney disease and attenuate EMT in renal tubular cells. Therefore, it is hypothesized that apelin might inhibit the EMT of podocytes through downregulating the expression and activation of TGFβ/Smad pathway in diabetic kidney diseases...
October 9, 2018: Cell Death & Disease
Nicolas Janus, Vincent Launay-Vacher, Gilbert Deray
The development of interventional radiology techniques regularly exposes patients to the potential renal toxocity of iodinated contrast media. Faced with this risk of nephrotoxicity, gadolinium-based contrast agents have long been considered as a safe alternative to iodinated contrast media, especially in sensitive or at risk patients. However, these gadolinium-based contrast agents are not devoid of nephrotoxicity and present another risk, a complication related to renal failure, the nephrogenic systemic fibrosis...
October 6, 2018: Néphrologie & Thérapeutique
Alla Mitrofanova, Judith Molina, Javier Varona Santos, Johanna Guzman, Ximena A Morales, G Michelle Ducasa, Jonathan Bryn, Alexis Sloan, Ion Volosenco, Jin-Ju Kim, Mengyuan Ge, Shamroop K Mallela, Matthias Kretzler, Sean Eddy, Sebastian Martini, Patricia Wahl, Santiago Pastori, Armando J Mendez, George W Burke, Sandra Merscher, Alessia Fornoni
Studies suggest that altered renal lipid metabolism plays a role in the pathogenesis of diabetic kidney disease and that genetic or pharmacological induction of cholesterol efflux protects from the development of diabetic kidney disease and focal segmental glomerulosclerosis (FSGS). Here we tested whether altered lipid metabolism contributes to renal failure in the Col4a3 knockout mouse model for Alport Syndrome. There was an eight-fold increase in the cholesterol content in renal cortexes of mice with Alport Syndrome...
October 6, 2018: Kidney International
Li-Ming Zhang, Jun Zhang, Ying Zhang, Lin Wang, Chang Fei, Zong-Wei Yi, Liang Dong
Interleukin (IL)-18 belongs to a rather large IL-1 gene family and is a proinflammatory cytokine. IL-18 plays important roles in lung injury. IL-18 binding protein (IL-18BP), a natural antagonist of IL-18, binds IL-18 with high affinity. IL-18BP is able to neutralize IL-18 biological activity and has a protective effect against renal fibrosis. The aim of this study was to evaluate the potential protective effect of IL-18BP on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and to illuminate the underlying mechanisms...
October 6, 2018: Biochemical and Biophysical Research Communications
Xiaolei Chen, Yiling Cao, Zheng Wang, Dongmei Zhang, Wanxin Tang
AIM: Hypertensive nephropathy (HTN) is one of the leading causes of end-stage renal disease and is closely associated with inflammation and tubule-interstitial fibrosis. The molecular mechanism underlying HTN remains unclear. This study utilized bioinformatic analysis to identify the novel gene targets for HTN. METHODS: We downloaded the microarray data of GSE99325 and GSE32591 from Gene Expression Omnibus. The dataset comprised 20 HTN and 15 normal samples. The differentially expressed genes (DEGs) were identified, and then gene ontology (GO) enrichment was performed, and a GO tree was constructed by using clusterProfiler and ClueGO...
October 8, 2018: Nephrology
Yu-Hsiang Chou, Tzong-Shinn Chu, Shuei-Liong Lin
Acute kidney injury (AKI) can increase the risk of developing incident chronic kidney disease (CKD). The severity, frequency and duration of AKI are crucial predictors of poor renal outcome. A repair process after AKI can be adaptive and kidney recovers completely after a mild injury. However, severe injury will lead to a maladaptive repair, which frequently progresses to nephron loss, vascular rarefaction, chronic inflammation and fibrosis. Although different mechanisms underlying AKI-CKD transition have been extensively discussed, no definite intervention has been proved effective to block or to retard the transition until recently...
October 2018: Nephrology
Ying Tang, Shiu-Kwong Mak, An P Xu, Hui-Yao Lan
Acute kidney injury (AKI) is characterized by both non-inflammatory and inflammatory process, and accumulating evidence has demonstrated that inflammation plays a key role in the pathogenesis and progression of AKI. C-reactive protein (CRP), an acute reactant produced by liver and many inflammatory cells, acts not only as an inflammation biomarker, but also as a pathogenic factor for AKI. Indeed, increased concentration of CRP is associated with poor outcome of varied etiologically related AKI patients. In recent years, the role of CRP is gradually recognized as an active participant in the pathogenesis and progression of AKI by exacerbating local inflammation, impairing the proliferation of damaged tubular epithelial cells and promoting fibrosis of injured renal tissue...
October 2018: Nephrology
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