scholarly journals Integrative Bioinformatics Analysis Provides Insight into the Molecular Mechanisms of Chronic Kidney Disease

2018 ◽  
Vol 43 (2) ◽  
pp. 568-581 ◽  
Author(s):  
Le-Ting Zhou ◽  
Shen Qiu ◽  
Lin-Li Lv ◽  
Zuo-Lin Li ◽  
Hong Liu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Insight Into

scholarly journals FO064INTEGRATIVE BIOINFORMATICS ANALYSIS PROVIDES INSIGHT INTO THE MOLECULAR MECHANISMS OF CHRONIC KIDNEY DISEASE

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i45-i46
Author(s):  
Le-Ting Zhou ◽  
Lin-Li Lv ◽  
Shen Qiu ◽  
Hong Liu ◽  
Ri-Ning Tang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Insight Into

scholarly journals Applying Proteomics and Integrative “Omics” Strategies to Decipher the Chronic Kidney Disease-Related Atherosclerosis

2021 ◽  
Vol 22 (14) ◽  
pp. 7492
Author(s):  
Joanna Tracz ◽  
Magdalena Luczak
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Premature Mortality ◽  
Protein Profiling ◽  
Bioinformatics Analyses ◽  
Increased Risk ◽  
High Prevalence ◽  
Insight Into ◽  
Integrative Omics

Patients with chronic kidney disease (CKD) are at increased risk of atherosclerosis and premature mortality, mainly due to cardiovascular events. However, well-known risk factors, which promote “classical” atherosclerosis are alone insufficient to explain the high prevalence of atherosclerosis-related to CKD (CKD-A). The complexity of the molecular mechanisms underlying the acceleration of CKD-A is still to be defied. To obtain a holistic picture of these changes, comprehensive proteomic approaches have been developed including global protein profiling followed by functional bioinformatics analyses of dysregulated pathways. Furthermore, proteomics surveys in combination with other “omics” techniques, i.e., transcriptomics and metabolomics as well as physiological assays provide a solid ground for interpretation of observed phenomena in the context of disease pathology. This review discusses the comprehensive application of various “omics” approaches, with emphasis on proteomics, to tackle the molecular mechanisms underlying CKD-A progression. We summarize here the recent findings derived from global proteomic approaches and underline the potential of utilizing integrative systems biology, to gain a deeper insight into the pathogenesis of CKD-A and other disorders.

scholarly journals Novel insight into perirenal adipose tissue: A neglected adipose depot linking cardiovascular and chronic kidney disease

2020 ◽  
Vol 11 (4) ◽  
pp. 115-125 ◽  
Author(s):  
Na Huang ◽  
En-Wen Mao ◽  
Ning-Ning Hou ◽  
Yong-Ping Liu ◽  
Fang Han ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Adipose Tissue ◽  
Kidney Disease ◽  
Perirenal Adipose Tissue ◽  
Adipose Depot ◽  
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MO448MICRORNAS IMPLICATED IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Laurent Metzinger
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Outcomes ◽  
Molecular Mechanisms ◽  
Neointimal Hyperplasia ◽  
Uremic Toxins ◽  
University Hospital ◽  
Transcriptional Level ◽  
Uremic Toxin ◽  
Ckd Stage

Abstract Background and Aims The gene program is controlled at the post-transcriptional level by the action of small non-coding RNAs known as microRNAs (miRNAs), short, single-stranded molecules that control mRNA stability or translational repression via base pairing with regions in the 3' untranslated region of their target mRNAs. Recently, considerable progress has been made to elucidate the roles of miRNAs in vascular pathogenesis and develop the use of miRNAs as biomarkers, and innovative drugs. We demonstrated during the last decade that miRNAs miR-126 and miR-223 are implicated in the course of chronic kidney disease (CKD) and cardiovascular damage. miR-223 expression is enhanced in vascular smooth muscle cells (VSMCs) subjected to an uremic toxin and also in aortas of a murine model of CKD. As restenosis is a common complication of angioplasty, in which neointimal hyperplasia results from migration of VSMCs into the vessel lumen we measured the effect of miR-223 modulation on restenosis in a rat model of carotid artery after balloon injury. We over-expressed and inhibited miR-223 expression using adenoviral vectors, coding a pre-miR-223 sequence or a sponge sequence, used to trap endogenous microRNA, respectively. We demonstrated that inhibiting miR-223 function significantly reduced neointimal hyperplasia by almost half in carotids. Thus down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty. We also correlated miR-126 and miR-223 expression with clinical outcomes in a large cohort of CKD patients, in collaboration with the University Hospital of Ghent (Belgium) and Ambroise Paré Hospital, France. We evaluated both miRNA’s link with all-cause mortality and cardiovascular and renal events over a 6-year follow-up period. The serum levels of miR-126 and miR-223 were decreased as CKD stage advanced, and patients with higher levels of miR-126 and miR-223 had a higher survival rate. Similar results were observed for cardiovascular and renal events. In conclusion, CKD is associated with a decrease in circulating miR-126 and miR-223 levels in CKD patients. We will also present links between several uremic toxin concentrations and miRNA concentration in the patients of this cohort. Finally, anemia is a common feature of CKD that is associated with cardiovascular disease and poor clinical outcomes. A mixture of uremic toxins accumulates in the blood of CKD patients during the course of the disease, and there is good evidence that they modulate erythropoiesis, explaining at least partly anemia. The exact molecular mechanisms implicated are however poorly understood, although recent progresses have been made to identify key components in the CKD process. We will present results on the effect of uremic toxins on erythropoiesis, having an impact on cell metabolism during this process. Taken together, our findings could be of interest to both researchers and clinicians working in the field since they might shed new light on the molecular mechanisms involved in the CKD process. MicroRNAs implicated in Chronic Kidney Disease Pr. Laurent Metzinger, UR-UPJV 4666 HEMATIM, CURS, Université de Picardie Jules Verne, CHU Amiens Sud, Avenue René Laënnec, Salouel, F-80054, Amiens, France. Tel: (+33) 22 82 53 56, Email: [email protected]

MO566THE BONE EXPRESSION OF WNT INHIBITORS IN THE EXPERIMENTAL MODEL OF EARLY CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Evdokia Bogdanova ◽  
Natalia Semenova ◽  
Olga Galkina ◽  
Irina Zubina ◽  
Olga Beresneva ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Experimental Model ◽  
Inorganic Phosphate ◽  
Molecular Mechanisms ◽  
Fibroblast Growth Factor 23 ◽  
Bone Matrix ◽  
Serum Levels ◽  
Chow Diet ◽  
Dickkopf 1

Abstract Background and Aims Molecular mechanisms implicated in the initial stages of inorganic phosphate (Pi) imbalance in chronic kidney disease (CKD) remain poorly understood.The aim of the study was to evaluate whether canonical Wnt pathway inhibitors (iWnt) involved in early response to Pi retention in CKD. Methods Mild CKD was induced by 3/4 nephrectomy (NE) in spontaneously hypertensive rats (SHR) fed rat chow diet containing 0.6 % phosphate. Controls were sham operated SHR (SO). Duration of experimental exposure (NE or SO) was 2 and 6 months. Serum levels of creatinine (Cr), inorganic phosphate (Pi), fractional Pi excretion (FEPi), intact parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), alfa-Klotho (KL), sclerostin (SOST) and Dickkopf-1 (DKK1) were measured. The following morphological characteristics by light microscopy of bone metaphysis and kidney tissues: the area of renal interstitial fibrosis (RF) (Masson's trichrome), bone matrix volume (MV), the active osteoblasts to trabecular cells number ratio (aOB/cells), eroded surface to bone surface ratio (ES/BS) (hematoxylin & eosin), and bone SOST and DKK1 proteins expression (by IHC) were analyzed and calculated quantitatively. Statistical comparisons among groups were performed using Mann–Whitney U-test and Kruskal-Wallis H-test. Results Serum Cr, RF and indices of Pi exchange in the experimental model corresponded to early CKD (Table). Pi elevated in NE6 suggestive for its renal retention. KL level decreased (Table) in all experimental groups vs control. No differences were observed in serum levels FGF23 (p=0.62) and PTH (p=0.63). Serum SOST and DKK1 levels were significantly higher in NE6 group compared to SO6 (Table). The bone SOST and DKK1 expression increased in NE6 compared to SO6 (Figure). aOB/cells were lower in NE2, SO6 and NE6 vs SO2 (all p-values<=0.041). ES/BS increased in NE2 (vs SO2) while being lowest in NE6 and SO6 animals (Table). SOST and DKK1 metaphyseal expression increased in NE6 compared to SO2, SO6, NE2 (Figure). Osteocyte SOST expression increased in SO6 compared to SO2 and NE2 without differences in later groups. Osteoblast SOST expression was also higher in SO6 vs SO2 (Figure). Conclusion Increased serum levels of sclerostin and Dickkopf-1 and their bone expression are apparent in early stages of experimental CKD associating with hyperphosphatemia. Alterations of bone resorption and osteoblast depopulation occurred before the increase of serum Pi likely reflecting incipient stages of renal Pi retention. These molecular and cellular events seem to be independent of systemic FGF23 and PTH response.

scholarly journals The renal microcirculation in chronic kidney disease: novel diagnostic methods and therapeutic perspectives

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shulin Li ◽  
Fei Wang ◽  
Dong Sun
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Molecular Mechanisms ◽  
Leukocyte Adhesion ◽  
Diagnostic Methods ◽  
Mesenchymal Transition ◽  
Microvascular Injury ◽  
Renal Microcirculation

AbstractChronic kidney disease (CKD) affects 8–16% of the population worldwide and is characterized by fibrotic processes. Understanding the cellular and molecular mechanisms underpinning renal fibrosis is critical to the development of new therapeutics. Microvascular injury is considered an important contributor to renal progressive diseases. Vascular endothelium plays a significant role in responding to physical and chemical signals by generating factors that help maintain normal vascular tone, inhibit leukocyte adhesion and platelet aggregation, and suppress smooth muscle cell proliferation. Loss of the rich capillary network results in endothelial dysfunction, hypoxia, and inflammatory and oxidative effects and further leads to the imbalance of pro- and antiangiogenic factors, endothelial cell apoptosis and endothelial-mesenchymal transition. New techniques, including both invasive and noninvasive techniques, offer multiple methods to observe and monitor renal microcirculation and guide targeted therapeutic strategies. A better understanding of the role of endothelium in CKD will help in the development of effective interventions for renal microcirculation improvement. This review focuses on the role of microvascular injury in CKD, the methods to detect microvessels and the novel treatments to ameliorate renal fibrosis.

scholarly journals Deeper insight into chronic kidney disease-related atherosclerosis: comparative proteomic studies of blood plasma using 2DE and mass spectrometry

2015 ◽  
Vol 13 (1) ◽  
pp. 20 ◽  
Author(s):  
Magdalena Luczak ◽  
Dorota Formanowicz ◽  
Łukasz Marczak ◽  
Elżbieta Pawliczak ◽  
Maria Wanic-Kossowska ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Blood Plasma ◽  
Insight Into
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