scholarly journals Role of Chemokine (C–X–C Motif) Ligand 10 (CXCL10) in Renal Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Jie Gao ◽  
Lingling Wu ◽  
Siyang Wang ◽  
Xiangmei Chen
Keyword(s):  
Kidney Disease ◽  
Mesangial Cells ◽  
Human Kidney ◽  
Inflammatory Cells ◽  
Prognostic Indicator ◽  
Renal Diseases ◽  
Inflammatory Conditions ◽  
Potential Biomarker ◽  
Inducible Protein

Chemokine C–X–C ligand 10 (CXCL10), also known as interferon-γ-inducible protein 10 (IP-10), exerts biological function mainly through binding to its specific receptor, CXCR3. Studies have shown that renal resident mesangial cells, renal tubular epithelial cells, podocytes, endothelial cells, and infiltrating inflammatory cells express CXCL10 and CXCR3 under inflammatory conditions. In the last few years, strong experimental and clinical evidence has indicated that CXCL10 is involved in the development of renal diseases through the chemoattraction of inflammatory cells and facilitation of cell growth and angiostatic effects. In addition, CXCL10 has been shown to be a significant biomarker of disease severity, and it can be used as a prognostic indicator for a variety of renal diseases, such as renal allograft dysfunction and lupus nephritis. In this review, we summarize the structures and biological functions of CXCL10 and CXCR3, focusing on the important role of CXCL10 in the pathogenesis of kidney disease, and provide a theoretical basis for CXCL10 as a potential biomarker and therapeutic target in human kidney disease.

scholarly journals Toll-Like Receptor as a Potential Biomarker in Renal Diseases

2020 ◽  
Vol 21 (18) ◽  
pp. 6712
Author(s):  
Sebastian Mertowski ◽  
Paulina Lipa ◽  
Izabela Morawska ◽  
Paulina Niedźwiedzka-Rystwej ◽  
Dominika Bębnowska ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Immunoglobulin A ◽  
Response To Treatment ◽  
Renal Diseases ◽  
Toll Like Receptor ◽  
Progressive Development ◽  
Non Invasive ◽  
Potential Marker ◽  
Potential Biomarker

One of the major challenges faced by modern nephrology is the identification of biomarkers associated with histopathological patterns or defined pathogenic mechanisms that may assist in the non-invasive diagnosis of kidney disease, particularly glomerulopathy. The identification of such molecules may allow prognostic subgroups to be established based on the type of disease, thereby predicting response to treatment or disease relapse. Advances in understanding the pathogenesis of diseases, such as membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis, IgA (immunoglobulin A) nephropathy, and diabetic nephropathy, along with the progressive development and standardization of plasma and urine proteomics techniques, have facilitated the identification of an increasing number of molecules that may be useful for these purposes. The growing number of studies on the role of TLR (toll-like receptor) receptors in the pathogenesis of kidney disease forces contemporary researchers to reflect on these molecules, which may soon join the group of renal biomarkers and become a helpful tool in the diagnosis of glomerulopathy. In this article, we conducted a thorough review of the literature on the role of TLRs in the pathogenesis of glomerulopathy. The role of TLR receptors as potential marker molecules for the development of neoplastic diseases is emphasized more and more often, as prognostic factors in diseases on several epidemiological backgrounds.

scholarly journals Phosphorylation of key podocyte proteins and the association with proteinuric kidney disease

2020 ◽  
Vol 319 (2) ◽  
pp. F284-F291 ◽  
Author(s):  
Di Feng
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Human Kidney ◽  
Future Directions ◽  
Genetic Studies ◽  
New Therapies ◽  
Podocyte Proteins

Podocyte dysfunction contributes to proteinuric chronic kidney disease. A number of key proteins are essential for podocyte function, including nephrin, podocin, CD2-associated protein (CD2AP), synaptopodin, and α-actinin-4 (ACTN4). Although most of these proteins were first identified through genetic studies associated with human kidney disease, subsequent studies have identified phosphorylation of these proteins as an important posttranslational event that regulates their function. In this review, a brief overview of the function of these key podocyte proteins is provided. Second, the role of phosphorylation in regulating the function of these proteins is described. Third, the association between these phosphorylation pathways and kidney disease is reviewed. Finally, challenges and future directions in studying phosphorylation are discussed. Better characterization of these phosphorylation pathways and others yet to be discovered holds promise for translating this knowledge into new therapies for patients with proteinuric chronic kidney disease.

scholarly journals The Key Role of Epithelial to Mesenchymal Transition (EMT) in Hypertensive Kidney Disease

2019 ◽  
Vol 20 (14) ◽  
pp. 3567 ◽  
Author(s):  
Teresa Seccia ◽  
Brasilina Caroccia ◽  
Maria Piazza ◽  
Gian Paolo Rossi
Keyword(s):  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Renal Diseases ◽  
Hypertensive Nephropathy ◽  
Mesenchymal Transition ◽  
Afferent Arterioles ◽  
Stage Renal Disease ◽  
End Stage

Accumulating evidence indicates that epithelial-to-mesenchymal transition (EMT), originally described as a key process for organ development and metastasis budding in cancer, plays a key role in the development of renal fibrosis in several diseases, including hypertensive nephroangiosclerosis. We herein reviewed the concept of EMT and its role in renal diseases, with particular focus on hypertensive kidney disease, the second leading cause of end-stage renal disease after diabetes mellitus. After discussing the pathophysiology of hypertensive nephropathy, the ‘classic’ view of hypertensive nephrosclerosis entailing hyalinization, and sclerosis of interlobular and afferent arterioles, we examined the changes occurring in the glomerulus and tubulo-interstitium and the studies that investigated the role of EMT and its molecular mechanisms in hypertensive kidney disease. Finally, we examined the reasons why some studies failed to provide solid evidence for renal EMT in hypertension.

Adhesion of Cultured Human Kidney Mesangial Cells to Native Entactin: Role of Integrin Receptors

1998 ◽  
Vol 5 (3) ◽  
pp. 237-248 ◽  
Author(s):  
Xiang-Yan Yi ◽  
Elizabeth A. Wayner ◽  
Youngki Kim ◽  
ALFRED J. FISH
Keyword(s):  
Mesangial Cells ◽  
Human Kidney ◽  
Integrin Receptors

Role of hypoxia‐inducible factor 1α as a potential biomarker for renal diseases—A systematic review

2019 ◽  
Vol 37 (6) ◽  
pp. 443-451 ◽  
Author(s):  
Jéssica Freitas Araújo Encinas ◽  
Carlos Henrique Foncesca ◽  
Matheus Moreira Perez ◽  
Diogo Pimenta Simões ◽  
Beatriz Costa Aguiar Alves ◽  
...  
Keyword(s):  
Systematic Review ◽  
Hypoxia Inducible Factor ◽  
Renal Diseases ◽  
Hypoxia Inducible Factor 1Α ◽  
Potential Biomarker

scholarly journals Autophagy in Immune-Related Renal Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Xin Ye ◽  
Xu-jie Zhou ◽  
Hong Zhang
Keyword(s):  
Diabetic Nephropathy ◽  
Immune Cells ◽  
Mesangial Cells ◽  
Pathological Process ◽  
Regulatory Mechanisms ◽  
Renal Diseases ◽  
Tubular Epithelial Cells ◽  
Biology Process ◽  
Glomerular Capillaries

Autophagy is an important biology process, central to the maintenance of biology process in both physiological and pathological situations. It is regarded as a “double-edged sword”—exerting both protective and/or detrimental effects. These two-way effects are observed in immune cells as well as renal resident cells, including podocytes, mesangial cells, tubular epithelial cells, and endothelial cells of the glomerular capillaries. Mounting evidence suggests that autophagy is implicated in the pathological process of various immune-related renal diseases (IRRDs) as well as the kidney that underwent transplantation. Here, we provide an overview of the pathological role of autophagy in IRRDs, including lupus nephritis, IgA nephropathy, membrane nephropathy, ANCA-associated nephritis, and diabetic nephropathy. The understanding of the pathogenesis and regulatory mechanisms of autophagy in these renal diseases may lead to the identification of new diagnostic targets and refined therapeutic modulation.

scholarly journals Pathogenic and protective role of macrophages in kidney disease

2013 ◽  
Vol 305 (1) ◽  
pp. F3-F11 ◽  
Author(s):  
Qi Cao ◽  
Yiping Wang ◽  
David C. H. Harris
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
Kidney Tissue ◽  
Human Kidney ◽  
Protective Role ◽  
Therapeutic Use ◽  
Disease Type ◽  
Dual Role ◽  
Murine Models

Macrophages (MΦ) are located throughout kidney tissue, where they play important roles in homeostasis, surveillance, tolerance, and cytoprotection. MΦ are highly heterogeneous cells and exhibit distinct phenotypic and functional characteristics depending on their microenvironment and the disease type and stage. Recent studies have identified a dual role for MΦ in several murine models of kidney disease. In this review, we discuss the pathogenic and protective roles of the various MΦ subsets in experimental and human kidney diseases and summarize current progress toward the therapeutic use of MΦ in kidney diseases.

scholarly journals Cytoprotective role of heme oxygenase (HO)-1 in human kidney with various renal diseases

2001 ◽  
Vol 60 (5) ◽  
pp. 1858-1866 ◽  
Author(s):  
Kayoko Morimoto ◽  
Kazuhide Ohta ◽  
Akihiro Yachie ◽  
Yonghong Yang ◽  
Masaki Shimizu ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Human Kidney ◽  
Renal Diseases

scholarly journals Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Qiaoyan Guo ◽  
Xiaoxia Li ◽  
Hongbo Han ◽  
Chaoyuan Li ◽  
Shujun Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Gene Promoter ◽  
Renal Diseases ◽  
Lysine Methylation ◽  
Histone Lysine Methylation ◽  
Histone Lysine ◽  
Chronic Renal Diseases

Transforming growth factor beta1- (TGF-β1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-β1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-β1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-β1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-β1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-β1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.

scholarly journals Critical Role for AMPK in Metabolic Disease-Induced Chronic Kidney Disease

2020 ◽  
Vol 21 (21) ◽  
pp. 7994 ◽  
Author(s):  
Florian Juszczak ◽  
Nathalie Caron ◽  
Anna V. Mathew ◽  
Anne-Emilie Declèves
Keyword(s):  
Metabolic Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mammalian Cells ◽  
Critical Role ◽  
Public Health Problem ◽  
Nutrient Sensing ◽  
Renal Diseases ◽  
Renal Cells

Chronic kidney disease (CKD) is prevalent in 9.1% of the global population and is a significant public health problem associated with increased morbidity and mortality. CKD is associated with highly prevalent physiological and metabolic disturbances such as hypertension, obesity, insulin resistance, cardiovascular disease, and aging, which are also risk factors for CKD pathogenesis and progression. Podocytes and proximal tubular cells of the kidney strongly express AMP-activated protein kinase (AMPK). AMPK plays essential roles in glucose and lipid metabolism, cell survival, growth, and inflammation. Thus, metabolic disease-induced renal diseases like obesity-related and diabetic chronic kidney disease demonstrate dysregulated AMPK in the kidney. Activating AMPK ameliorates the pathological and phenotypical features of both diseases. As a metabolic sensor, AMPK regulates active tubular transport and helps renal cells to survive low energy states. AMPK also exerts a key role in mitochondrial homeostasis and is known to regulate autophagy in mammalian cells. While the nutrient-sensing role of AMPK is critical in determining the fate of renal cells, the role of AMPK in kidney autophagy and mitochondrial quality control leading to pathology in metabolic disease-related CKD is not very clear and needs further investigation. This review highlights the crucial role of AMPK in renal cell dysfunction associated with metabolic diseases and aims to expand therapeutic strategies by understanding the molecular and cellular processes underlying CKD.

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